TY  - JOUR
AU  - Lukić, Nikola
AU  - Mačvanin, Mirjana T.
AU  - Gluvić, Zoran
AU  - Rizzo, Manfredi
AU  - Radak, Đorđe
AU  - Suri, Jasjit S.
AU  - Isenović, Esma R.
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12022
AB  - Type 2 diabetes mellitus (T2DM) has become a worldwide concern in recent years, primarily in highly developed Western societies. T2DM causes systemic complications, such as atherosclerotic heart disease, ischemic stroke, peripheral artery disease, kidney failure, and diabetes-related maculopathy and retinopathy. The growing number of T2DM patients and the treatment of long-term T2DM-related complications pressurize and exhaust public healthcare systems. As a result, strategies for combating T2DM and developing novel drugs are critical global public health requirements. Aside from preventive measures, which are still the most effective way to prevent T2DM, novel and highly effective therapies are emerging. In the spotlight of next-generation T2DM treatment, sodium-glucose co-transporter 2 (SGLT-2) inhibitors are promoted as the most efficient perspective therapy. SGLT-2 inhibitors (SGLT2i) include phlorizin derivatives, such as canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin. SGLT-2, along with SGLT-1, is a member of the SGLT family of proteins that play a role in glucose absorption via active transport mediated by Na+ /K+ ATPase. SGLT-2 is only found in the kidney, specifically the proximal tubule, and is responsible for more than 90% glucose absorption. Inhibition of SGLT-2 reduces glucose absorption, and consequently increases urinary glucose excretion, decreasing blood glucose levels. Thus, the inhibition of SGLT-2 activity ultimately alleviates T2DM-related symptoms and prevents or delays systemic T2DM-associated chronic complications. This review aimed to provide a more detailed understanding of the effects of SGLT2i responsible for the acute improvement in blood glucose regulation, a prerequisite for T2DM-associated cardiovascular complications control.
T2  - Current Medicinal Chemistry
T1  - SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus
VL  - 31
DO  - 10.2174/0109298673251493231011192520
ER  - 

@article{
author = "Lukić, Nikola and Mačvanin, Mirjana T. and Gluvić, Zoran and Rizzo, Manfredi and Radak, Đorđe and Suri, Jasjit S. and Isenović, Esma R.",
year = "2023",
abstract = "Type 2 diabetes mellitus (T2DM) has become a worldwide concern in recent years, primarily in highly developed Western societies. T2DM causes systemic complications, such as atherosclerotic heart disease, ischemic stroke, peripheral artery disease, kidney failure, and diabetes-related maculopathy and retinopathy. The growing number of T2DM patients and the treatment of long-term T2DM-related complications pressurize and exhaust public healthcare systems. As a result, strategies for combating T2DM and developing novel drugs are critical global public health requirements. Aside from preventive measures, which are still the most effective way to prevent T2DM, novel and highly effective therapies are emerging. In the spotlight of next-generation T2DM treatment, sodium-glucose co-transporter 2 (SGLT-2) inhibitors are promoted as the most efficient perspective therapy. SGLT-2 inhibitors (SGLT2i) include phlorizin derivatives, such as canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin. SGLT-2, along with SGLT-1, is a member of the SGLT family of proteins that play a role in glucose absorption via active transport mediated by Na+ /K+ ATPase. SGLT-2 is only found in the kidney, specifically the proximal tubule, and is responsible for more than 90% glucose absorption. Inhibition of SGLT-2 reduces glucose absorption, and consequently increases urinary glucose excretion, decreasing blood glucose levels. Thus, the inhibition of SGLT-2 activity ultimately alleviates T2DM-related symptoms and prevents or delays systemic T2DM-associated chronic complications. This review aimed to provide a more detailed understanding of the effects of SGLT2i responsible for the acute improvement in blood glucose regulation, a prerequisite for T2DM-associated cardiovascular complications control.",
journal = "Current Medicinal Chemistry",
title = "SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus",
volume = "31",
doi = "10.2174/0109298673251493231011192520"
}

Lukić, N., Mačvanin, M. T., Gluvić, Z., Rizzo, M., Radak, Đ., Suri, J. S.,& Isenović, E. R.. (2023). SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus. in Current Medicinal Chemistry, 31.
https://doi.org/10.2174/0109298673251493231011192520

Lukić N, Mačvanin MT, Gluvić Z, Rizzo M, Radak Đ, Suri JS, Isenović ER. SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus. in Current Medicinal Chemistry. 2023;31.
doi:10.2174/0109298673251493231011192520 .

Lukić, Nikola, Mačvanin, Mirjana T., Gluvić, Zoran, Rizzo, Manfredi, Radak, Đorđe, Suri, Jasjit S., Isenović, Esma R., "SGLT-2 Inhibitors: The Next-generation Treatment for Type 2 Diabetes Mellitus" in Current Medicinal Chemistry, 31 (2023),
https://doi.org/10.2174/0109298673251493231011192520 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Gluvić, Zoran
AU  - Banjac, Katarina
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10756
AB  - Cardiometabolic diseases (CMD) are a direct consequence of modern living and contribute to the development of multisystem diseases such as cardiovascular diseases and diabetes mellitus (DM). CMD has reached epidemic proportions worldwide. A sodium pump (Na + /K + -ATPase) is found in most eukaryotic cells’ membrane and controls many essential cellular functions directly or indirectly. This ion transporter and its isoforms are important in the pathogenesis of some pathological processes, including CMD. The structure and function of Na + /K + -ATPase, its expression and distribution in tissues, and its interactions with known ligands such as cardiotonic steroids and other suspected endogenous regulators are discussed in this review. In addition, we reviewed recent literature data related to the involvement of Na + /K + -ATPase activity dysfunction in CMD, focusing on the Na + /K + -ATPase as a potential therapeutic target in CMD.
T2  - Frontiers in Endocrinology
T1  - The Na+/K+-ATPase: A potential therapeutic target in cardiometabolic diseases
VL  - 14
DO  - 10.3389/fendo.2023.1150171
ER  - 

@article{
author = "Obradović, Milan M. and Sudar-Milovanović, Emina and Gluvić, Zoran and Banjac, Katarina and Rizzo, Manfredi and Isenović, Esma R.",
year = "2023",
abstract = "Cardiometabolic diseases (CMD) are a direct consequence of modern living and contribute to the development of multisystem diseases such as cardiovascular diseases and diabetes mellitus (DM). CMD has reached epidemic proportions worldwide. A sodium pump (Na + /K + -ATPase) is found in most eukaryotic cells’ membrane and controls many essential cellular functions directly or indirectly. This ion transporter and its isoforms are important in the pathogenesis of some pathological processes, including CMD. The structure and function of Na + /K + -ATPase, its expression and distribution in tissues, and its interactions with known ligands such as cardiotonic steroids and other suspected endogenous regulators are discussed in this review. In addition, we reviewed recent literature data related to the involvement of Na + /K + -ATPase activity dysfunction in CMD, focusing on the Na + /K + -ATPase as a potential therapeutic target in CMD.",
journal = "Frontiers in Endocrinology",
title = "The Na+/K+-ATPase: A potential therapeutic target in cardiometabolic diseases",
volume = "14",
doi = "10.3389/fendo.2023.1150171"
}

Obradović, M. M., Sudar-Milovanović, E., Gluvić, Z., Banjac, K., Rizzo, M.,& Isenović, E. R.. (2023). The Na+/K+-ATPase: A potential therapeutic target in cardiometabolic diseases. in Frontiers in Endocrinology, 14.
https://doi.org/10.3389/fendo.2023.1150171

Obradović MM, Sudar-Milovanović E, Gluvić Z, Banjac K, Rizzo M, Isenović ER. The Na+/K+-ATPase: A potential therapeutic target in cardiometabolic diseases. in Frontiers in Endocrinology. 2023;14.
doi:10.3389/fendo.2023.1150171 .

Obradović, Milan M., Sudar-Milovanović, Emina, Gluvić, Zoran, Banjac, Katarina, Rizzo, Manfredi, Isenović, Esma R., "The Na+/K+-ATPase: A potential therapeutic target in cardiometabolic diseases" in Frontiers in Endocrinology, 14 (2023),
https://doi.org/10.3389/fendo.2023.1150171 . .

TY  - JOUR
AU  - Mačvanin, Mirjana
AU  - Gluvić, Zoran
AU  - Klisić, Aleksandra
AU  - Manojlović, Mia
AU  - Suri, Jasjit
AU  - Rizzo, Manfredi
AU  - Isenović, Esma
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/12021
AB  - Cardiovascular disease (CDV) represents the major cause of death globally. Atherosclerosis, as the primary cause of CVD, is a chronic immune-inflammatory disorder with complex multifactorial pathophysiology encompassing oxidative stress, enhanced immune-inflammatory cascade, endothelial dysfunction, and thrombosis. An initiating event in atherosclerosis is the subendothelial accumulation of low-density lipoprotein (LDL), followed by the localization of macrophages to fatty deposits on blood vessel walls, forming lipid-laden macrophages (foam cells) that secrete compounds involved in plaque formation. Given the fact that foam cells are one of the key culprits that underlie the pathophysiology of atherosclerosis, special attention has been paid to the investigation of the efficient therapeutic approach to overcome the dysregulation of metabolism of cholesterol in macrophages, decrease the foam cell formation and/or to force its degradation. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a secretory serine proteinase that has emerged as a significant regulator of the lipid metabolism pathway. PCSK9 activation leads to the degradation of LDL receptors (LDLRs), increasing LDL cholesterol (LDL-C) levels in the circulation. PCSK9 pathway dysregulation has been identified as one of the mechanisms involved in atherosclerosis. In addition, microRNAs (miRNAs) are investigated as important epigenetic factors in the pathophysiology of atherosclerosis and dysregulation of lipid metabolism. This review article summarizes the recent findings connecting the role of PCSK9 in atherosclerosis and the involvement of various miRNAs in regulating the expression of PCSK9-related genes. We also discuss PCSK9 pathway-targeting therapeutic interventions based on PCSK9 inhibition, miRNA levels manipulation by therapeutic agents, and the most recent advances in PSCK9 gene editing using CRISPR/Cas9 platform, meganuclease, and base editors.
T2  - Current Medicinal Chemistry
T1  - The Link between miRNAs and PCKS9 in Atherosclerosis
VL  - 31
DO  - 10.2174/0109298673262124231102042914
ER  - 

@article{
author = "Mačvanin, Mirjana and Gluvić, Zoran and Klisić, Aleksandra and Manojlović, Mia and Suri, Jasjit and Rizzo, Manfredi and Isenović, Esma",
year = "2023",
abstract = "Cardiovascular disease (CDV) represents the major cause of death globally. Atherosclerosis, as the primary cause of CVD, is a chronic immune-inflammatory disorder with complex multifactorial pathophysiology encompassing oxidative stress, enhanced immune-inflammatory cascade, endothelial dysfunction, and thrombosis. An initiating event in atherosclerosis is the subendothelial accumulation of low-density lipoprotein (LDL), followed by the localization of macrophages to fatty deposits on blood vessel walls, forming lipid-laden macrophages (foam cells) that secrete compounds involved in plaque formation. Given the fact that foam cells are one of the key culprits that underlie the pathophysiology of atherosclerosis, special attention has been paid to the investigation of the efficient therapeutic approach to overcome the dysregulation of metabolism of cholesterol in macrophages, decrease the foam cell formation and/or to force its degradation. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a secretory serine proteinase that has emerged as a significant regulator of the lipid metabolism pathway. PCSK9 activation leads to the degradation of LDL receptors (LDLRs), increasing LDL cholesterol (LDL-C) levels in the circulation. PCSK9 pathway dysregulation has been identified as one of the mechanisms involved in atherosclerosis. In addition, microRNAs (miRNAs) are investigated as important epigenetic factors in the pathophysiology of atherosclerosis and dysregulation of lipid metabolism. This review article summarizes the recent findings connecting the role of PCSK9 in atherosclerosis and the involvement of various miRNAs in regulating the expression of PCSK9-related genes. We also discuss PCSK9 pathway-targeting therapeutic interventions based on PCSK9 inhibition, miRNA levels manipulation by therapeutic agents, and the most recent advances in PSCK9 gene editing using CRISPR/Cas9 platform, meganuclease, and base editors.",
journal = "Current Medicinal Chemistry",
title = "The Link between miRNAs and PCKS9 in Atherosclerosis",
volume = "31",
doi = "10.2174/0109298673262124231102042914"
}

Mačvanin, M., Gluvić, Z., Klisić, A., Manojlović, M., Suri, J., Rizzo, M.,& Isenović, E.. (2023). The Link between miRNAs and PCKS9 in Atherosclerosis. in Current Medicinal Chemistry, 31.
https://doi.org/10.2174/0109298673262124231102042914

Mačvanin M, Gluvić Z, Klisić A, Manojlović M, Suri J, Rizzo M, Isenović E. The Link between miRNAs and PCKS9 in Atherosclerosis. in Current Medicinal Chemistry. 2023;31.
doi:10.2174/0109298673262124231102042914 .

Mačvanin, Mirjana, Gluvić, Zoran, Klisić, Aleksandra, Manojlović, Mia, Suri, Jasjit, Rizzo, Manfredi, Isenović, Esma, "The Link between miRNAs and PCKS9 in Atherosclerosis" in Current Medicinal Chemistry, 31 (2023),
https://doi.org/10.2174/0109298673262124231102042914 . .

TY  - JOUR
AU  - Gluvić, Zoran
AU  - Zafirović, Sonja
AU  - Obradović, Milan M.
AU  - Sudar-Milovanović, Emina
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10409
AB  - Thyroid hormones (TH) have a significant impact on cellular oxidative metabolism. Besides that,they maintain vascular homeostasis by positive effects on endothelial and vascular smooth muscle cells. Subclinical(SCH) and clinical (CH) hypothyroidism influences target organs by changing their morphology andfunction and impaired blood and oxygen supply induced by accelerated atherosclerosis. The increased risk ofacceleration and extension of atherosclerosis in patients with SCH and CH could be explained by dyslipidemia,diastolic hypertension, increased arterial stiffness, endothelial dysfunction, and altered blood coagulation. Instabilityof atherosclerotic plaque in hypothyroidism could cause excessive activity of the elements of innateimmunity, which are characterized by the significant presence of macrophages in atherosclerotic plaques, increasednuclear factor kappa B (NFkB) expression, and elevated levels of tumor necrosis factor α (TNF-α) andmatrix metalloproteinase (MMP) 9, with reduced interstitial collagen; all of them together creates inflammationmilieu, resulting in plaque rupture. Optimal substitution by levothyroxine (LT4) restores biochemical euthyroidism.In postmenopausal women and elderly patients with hypothyroidism and associated vascularcomorbidity, excessive LT4 substitution could lead to atrial rhythm disorders and osteoporosis. Therefore, it isof interest to maintain thyroid-stimulating hormone (TSH) levels in the reference range, thus eliminating thedeleterious effects of lower or higher TSH levels on the cardiovascular system. This review summarizes the recentliterature on subclinical and clinical hypothyroidism and atherosclerotic cardiovascular disease and discussesthe effects of LT4 replacement therapy on restoring biochemical euthyroidism and atherosclerosis processes.
T2  - Current Pharmaceutical Design
T1  - Hypothyroidism and Risk of Cardiovascular Disease
VL  - 28
IS  - 25
SP  - 2065
EP  - 2072
DO  - 10.2174/1381612828666220620160516
ER  - 

@article{
author = "Gluvić, Zoran and Zafirović, Sonja and Obradović, Milan M. and Sudar-Milovanović, Emina and Rizzo, Manfredi and Isenović, Esma R.",
year = "2022",
abstract = "Thyroid hormones (TH) have a significant impact on cellular oxidative metabolism. Besides that,they maintain vascular homeostasis by positive effects on endothelial and vascular smooth muscle cells. Subclinical(SCH) and clinical (CH) hypothyroidism influences target organs by changing their morphology andfunction and impaired blood and oxygen supply induced by accelerated atherosclerosis. The increased risk ofacceleration and extension of atherosclerosis in patients with SCH and CH could be explained by dyslipidemia,diastolic hypertension, increased arterial stiffness, endothelial dysfunction, and altered blood coagulation. Instabilityof atherosclerotic plaque in hypothyroidism could cause excessive activity of the elements of innateimmunity, which are characterized by the significant presence of macrophages in atherosclerotic plaques, increasednuclear factor kappa B (NFkB) expression, and elevated levels of tumor necrosis factor α (TNF-α) andmatrix metalloproteinase (MMP) 9, with reduced interstitial collagen; all of them together creates inflammationmilieu, resulting in plaque rupture. Optimal substitution by levothyroxine (LT4) restores biochemical euthyroidism.In postmenopausal women and elderly patients with hypothyroidism and associated vascularcomorbidity, excessive LT4 substitution could lead to atrial rhythm disorders and osteoporosis. Therefore, it isof interest to maintain thyroid-stimulating hormone (TSH) levels in the reference range, thus eliminating thedeleterious effects of lower or higher TSH levels on the cardiovascular system. This review summarizes the recentliterature on subclinical and clinical hypothyroidism and atherosclerotic cardiovascular disease and discussesthe effects of LT4 replacement therapy on restoring biochemical euthyroidism and atherosclerosis processes.",
journal = "Current Pharmaceutical Design",
title = "Hypothyroidism and Risk of Cardiovascular Disease",
volume = "28",
number = "25",
pages = "2065-2072",
doi = "10.2174/1381612828666220620160516"
}

Gluvić, Z., Zafirović, S., Obradović, M. M., Sudar-Milovanović, E., Rizzo, M.,& Isenović, E. R.. (2022). Hypothyroidism and Risk of Cardiovascular Disease. in Current Pharmaceutical Design, 28(25), 2065-2072.
https://doi.org/10.2174/1381612828666220620160516

Gluvić Z, Zafirović S, Obradović MM, Sudar-Milovanović E, Rizzo M, Isenović ER. Hypothyroidism and Risk of Cardiovascular Disease. in Current Pharmaceutical Design. 2022;28(25):2065-2072.
doi:10.2174/1381612828666220620160516 .

Gluvić, Zoran, Zafirović, Sonja, Obradović, Milan M., Sudar-Milovanović, Emina, Rizzo, Manfredi, Isenović, Esma R., "Hypothyroidism and Risk of Cardiovascular Disease" in Current Pharmaceutical Design, 28, no. 25 (2022):2065-2072,
https://doi.org/10.2174/1381612828666220620160516 . .

TY  - JOUR
AU  - Mačvanin, Mirjana
AU  - Rizzo, Manfredi
AU  - Radovanović, Jelena N.
AU  - Sonmez, Alper
AU  - Paneni, Francesco
AU  - Isenović, Esma R.
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10569
AB  - (1) Background: Obesity is closely connected to the pathophysiology of cardiovascular diseases (CVDs). Excess fat accumulation is associated with metabolic malfunctions that disrupt cardiovascular homeostasis by activating inflammatory processes that recruit immune cells to the site of injury and reduce nitric oxide levels, resulting in increased blood pressure, endothelial cell migration, proliferation, and apoptosis. Adipose tissue produces adipokines, such as chemerin, that may alter immune responses, lipid metabolism, vascular homeostasis, and angiogenesis. (2) Methods: We performed PubMed and MEDLINE searches for articles with English abstracts published between 1997 (when the first report on chemerin identification was published) and 2022. The search retrieved original peer-reviewed articles analyzed in the context of the role of chemerin in CVDs, explicitly focusing on the most recent findings published in the past five years. (3) Results: This review summarizes up-to-date findings related to mechanisms of chemerin action, its role in the development and progression of CVDs, and novel strategies for developing chemerin-targeting therapeutic agents for treating CVDs. (4) Conclusions: Extensive evidence points to chemerin’s role in vascular inflammation, angiogenesis, and blood pressure modulation, which opens up exciting perspectives for developing chemerin-targeting therapeutic agents for the treatment of CVDs.
T2  - Biomedicines
T1  - Role of Chemerin in Cardiovascular Diseases
VL  - 10
IS  - 11
SP  - 2970
DO  - 10.3390/biomedicines10112970
ER  - 

@article{
author = "Mačvanin, Mirjana and Rizzo, Manfredi and Radovanović, Jelena N. and Sonmez, Alper and Paneni, Francesco and Isenović, Esma R.",
year = "2022",
abstract = "(1) Background: Obesity is closely connected to the pathophysiology of cardiovascular diseases (CVDs). Excess fat accumulation is associated with metabolic malfunctions that disrupt cardiovascular homeostasis by activating inflammatory processes that recruit immune cells to the site of injury and reduce nitric oxide levels, resulting in increased blood pressure, endothelial cell migration, proliferation, and apoptosis. Adipose tissue produces adipokines, such as chemerin, that may alter immune responses, lipid metabolism, vascular homeostasis, and angiogenesis. (2) Methods: We performed PubMed and MEDLINE searches for articles with English abstracts published between 1997 (when the first report on chemerin identification was published) and 2022. The search retrieved original peer-reviewed articles analyzed in the context of the role of chemerin in CVDs, explicitly focusing on the most recent findings published in the past five years. (3) Results: This review summarizes up-to-date findings related to mechanisms of chemerin action, its role in the development and progression of CVDs, and novel strategies for developing chemerin-targeting therapeutic agents for treating CVDs. (4) Conclusions: Extensive evidence points to chemerin’s role in vascular inflammation, angiogenesis, and blood pressure modulation, which opens up exciting perspectives for developing chemerin-targeting therapeutic agents for the treatment of CVDs.",
journal = "Biomedicines",
title = "Role of Chemerin in Cardiovascular Diseases",
volume = "10",
number = "11",
pages = "2970",
doi = "10.3390/biomedicines10112970"
}

Mačvanin, M., Rizzo, M., Radovanović, J. N., Sonmez, A., Paneni, F.,& Isenović, E. R.. (2022). Role of Chemerin in Cardiovascular Diseases. in Biomedicines, 10(11), 2970.
https://doi.org/10.3390/biomedicines10112970

Mačvanin M, Rizzo M, Radovanović JN, Sonmez A, Paneni F, Isenović ER. Role of Chemerin in Cardiovascular Diseases. in Biomedicines. 2022;10(11):2970.
doi:10.3390/biomedicines10112970 .

Mačvanin, Mirjana, Rizzo, Manfredi, Radovanović, Jelena N., Sonmez, Alper, Paneni, Francesco, Isenović, Esma R., "Role of Chemerin in Cardiovascular Diseases" in Biomedicines, 10, no. 11 (2022):2970,
https://doi.org/10.3390/biomedicines10112970 . .

TY  - JOUR
AU  - Rizzo, Manfredi
AU  - Abate, Nicola
AU  - Chandalia, Manisha
AU  - Rizvi, Ali A.
AU  - Giglio, Rosaria V.
AU  - Nikolić, Dragana
AU  - Gammazza, Antonella Marino
AU  - Barbagallo, Ignazio
AU  - Isenović, Esma R.
AU  - Banach, Maciej
AU  - Montalto, Giuseppe
AU  - Volti, Giovanni Li
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/508
AB  - Context: Liraglutide is a glucagon-like peptide-1 analog and glucose-lowering agent whose effects on cardiovascular risk markers have not been fully elucidated. Objective: We evaluated the effect of liraglutide on markers of oxidative stress, heme oxygenase-1 (HO-1), and plasma ghrelin levels in patients with type-2 diabetes mellitus (T2DM). Design and Setting: A prospective pilot study of 2 months duration has been performed at the Unit of Diabetes and Cardiovascular Prevention at University of Palermo, Italy. Patients and Intervention(s): Twenty subjects with T2DM (10 men and 10 women; meanage: 57 +/- 13 y) were treated with liraglutide sc (0.6 mg/d for 2 wk, followed by 1.2 mg/d) in addition to metformin (1500 mg/d orally) for 2 months. Patients with liver disorders or renal failure were excluded. Main Outcome Measure(s): Plasma ghrelin concentrations, oxidative stress markers, and heat-shock proteins, including HO-1 were assessed. Results: The addition of liraglutide resulted in a significant decrease in glycated hemoglobin (HbA1c) (8.5 +/- 0.4 vs 7.5 +/- 0.4%, P LT .0001). In addition, plasma ghrelin and glutathione concentrations increased (8.2 +/- 4.1 vs 13.6 +/- 7.3 pg/ml, P = .0007 and 0.36 +/- 0.06 vs 0.44 +/- 0.07 nmol/ml, P = .0002, respectively), whereas serum lipid hydroperoxides and HO-1 decreased (0.11 +/- 0.05 vs 0.04 +/- 0.07 pg/ml, P = .0487 and 7.7 +/- 7.7 vs 3.6 +/- 1.8 pg/ml, P = .0445, respectively). These changes were not correlated with changes in fasting glycemia or HbA1c. Conclusions: In a 2-months prospective pilot study, the addition of liraglutide to metformin resulted in improvement in oxidative stress as well as plasma ghrelin and HO-1 concentrations in patients with T2DM. These findings seemed to be independent of the known effects of liraglutide on glucose metabolism.
T2  - Journal of Clinical Endocrinology and Metabolism
T1  - Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study
VL  - 100
IS  - 2
SP  - 603
EP  - 606
DO  - 10.1210/jc.2014-2291
ER  - 

@article{
author = "Rizzo, Manfredi and Abate, Nicola and Chandalia, Manisha and Rizvi, Ali A. and Giglio, Rosaria V. and Nikolić, Dragana and Gammazza, Antonella Marino and Barbagallo, Ignazio and Isenović, Esma R. and Banach, Maciej and Montalto, Giuseppe and Volti, Giovanni Li",
year = "2015",
abstract = "Context: Liraglutide is a glucagon-like peptide-1 analog and glucose-lowering agent whose effects on cardiovascular risk markers have not been fully elucidated. Objective: We evaluated the effect of liraglutide on markers of oxidative stress, heme oxygenase-1 (HO-1), and plasma ghrelin levels in patients with type-2 diabetes mellitus (T2DM). Design and Setting: A prospective pilot study of 2 months duration has been performed at the Unit of Diabetes and Cardiovascular Prevention at University of Palermo, Italy. Patients and Intervention(s): Twenty subjects with T2DM (10 men and 10 women; meanage: 57 +/- 13 y) were treated with liraglutide sc (0.6 mg/d for 2 wk, followed by 1.2 mg/d) in addition to metformin (1500 mg/d orally) for 2 months. Patients with liver disorders or renal failure were excluded. Main Outcome Measure(s): Plasma ghrelin concentrations, oxidative stress markers, and heat-shock proteins, including HO-1 were assessed. Results: The addition of liraglutide resulted in a significant decrease in glycated hemoglobin (HbA1c) (8.5 +/- 0.4 vs 7.5 +/- 0.4%, P LT .0001). In addition, plasma ghrelin and glutathione concentrations increased (8.2 +/- 4.1 vs 13.6 +/- 7.3 pg/ml, P = .0007 and 0.36 +/- 0.06 vs 0.44 +/- 0.07 nmol/ml, P = .0002, respectively), whereas serum lipid hydroperoxides and HO-1 decreased (0.11 +/- 0.05 vs 0.04 +/- 0.07 pg/ml, P = .0487 and 7.7 +/- 7.7 vs 3.6 +/- 1.8 pg/ml, P = .0445, respectively). These changes were not correlated with changes in fasting glycemia or HbA1c. Conclusions: In a 2-months prospective pilot study, the addition of liraglutide to metformin resulted in improvement in oxidative stress as well as plasma ghrelin and HO-1 concentrations in patients with T2DM. These findings seemed to be independent of the known effects of liraglutide on glucose metabolism.",
journal = "Journal of Clinical Endocrinology and Metabolism",
title = "Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study",
volume = "100",
number = "2",
pages = "603-606",
doi = "10.1210/jc.2014-2291"
}

Rizzo, M., Abate, N., Chandalia, M., Rizvi, A. A., Giglio, R. V., Nikolić, D., Gammazza, A. M., Barbagallo, I., Isenović, E. R., Banach, M., Montalto, G.,& Volti, G. L.. (2015). Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study. in Journal of Clinical Endocrinology and Metabolism, 100(2), 603-606.
https://doi.org/10.1210/jc.2014-2291

Rizzo M, Abate N, Chandalia M, Rizvi AA, Giglio RV, Nikolić D, Gammazza AM, Barbagallo I, Isenović ER, Banach M, Montalto G, Volti GL. Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study. in Journal of Clinical Endocrinology and Metabolism. 2015;100(2):603-606.
doi:10.1210/jc.2014-2291 .

Rizzo, Manfredi, Abate, Nicola, Chandalia, Manisha, Rizvi, Ali A., Giglio, Rosaria V., Nikolić, Dragana, Gammazza, Antonella Marino, Barbagallo, Ignazio, Isenović, Esma R., Banach, Maciej, Montalto, Giuseppe, Volti, Giovanni Li, "Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study" in Journal of Clinical Endocrinology and Metabolism, 100, no. 2 (2015):603-606,
https://doi.org/10.1210/jc.2014-2291 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Stanimirović, Julijana
AU  - Rizzo, Manfredi
AU  - Resanović, Ivana
AU  - Soskić, Sanja S.
AU  - Jevremovic, Danimir
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/613
AB  - The assessment of cardiovascular risk and treatment of cardiovascular diseases are major public health issues worldwide. Inflammation is now recognized as a key regulatory process that links multiple risk factors for atherosclerosis. The substantial number of patients having cardiovascular events lack commonly established risk factors. The utility of high-sensitivity C-reactive protein (hsCRP), a circulating biomarker related to inflammation, may provide additional information in risk prediction. This review will consider the impact of hsCRP level on initiation of statin therapy.
T2  - Angiology
T1  - High-Sensitivity C-Reactive Protein and Statin Initiation
VL  - 66
IS  - 6
SP  - 503
EP  - 507
DO  - 10.1177/0003319714543000
ER  - 

@article{
author = "Trpković, Andreja and Stanimirović, Julijana and Rizzo, Manfredi and Resanović, Ivana and Soskić, Sanja S. and Jevremovic, Danimir and Isenović, Esma R.",
year = "2015",
abstract = "The assessment of cardiovascular risk and treatment of cardiovascular diseases are major public health issues worldwide. Inflammation is now recognized as a key regulatory process that links multiple risk factors for atherosclerosis. The substantial number of patients having cardiovascular events lack commonly established risk factors. The utility of high-sensitivity C-reactive protein (hsCRP), a circulating biomarker related to inflammation, may provide additional information in risk prediction. This review will consider the impact of hsCRP level on initiation of statin therapy.",
journal = "Angiology",
title = "High-Sensitivity C-Reactive Protein and Statin Initiation",
volume = "66",
number = "6",
pages = "503-507",
doi = "10.1177/0003319714543000"
}

Trpković, A., Stanimirović, J., Rizzo, M., Resanović, I., Soskić, S. S., Jevremovic, D.,& Isenović, E. R.. (2015). High-Sensitivity C-Reactive Protein and Statin Initiation. in Angiology, 66(6), 503-507.
https://doi.org/10.1177/0003319714543000

Trpković A, Stanimirović J, Rizzo M, Resanović I, Soskić SS, Jevremovic D, Isenović ER. High-Sensitivity C-Reactive Protein and Statin Initiation. in Angiology. 2015;66(6):503-507.
doi:10.1177/0003319714543000 .

Trpković, Andreja, Stanimirović, Julijana, Rizzo, Manfredi, Resanović, Ivana, Soskić, Sanja S., Jevremovic, Danimir, Isenović, Esma R., "High-Sensitivity C-Reactive Protein and Statin Initiation" in Angiology, 66, no. 6 (2015):503-507,
https://doi.org/10.1177/0003319714543000 . .

TY  - JOUR
AU  - Abate, Nicola
AU  - Sallam, Hanaa S.
AU  - Rizzo, Manfredi
AU  - Nikolić, Dragana
AU  - Obradović, Milan M.
AU  - Bjelogrlic, Predrag
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/56
AB  - Resistin is an adipocyte-and monocyte-derived cytokine which has been implicated in the modulation of insulin action, energy, glucose and lipid homeostasis. Resistin has been associated with insulin resistance and many of its known complications. As a molecular link between metabolic signals, inflammation, and vascular dysfunction, resistin can be proposed as playing a significant role in the heightened inflammatory state induced by metabolic stress linked to excessive caloric intake, thus contributing to the risk for metabolic syndrome (MetS), type 2 diabetes (T2DM), and cardiovascular diseases (CVD). In this review, we highlighted the role of resistin, as an inflammatory cytokine, in the development of CVD, T2DM and the MetS.
T2  - Current Pharmaceutical Design
T1  - Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome
VL  - 20
IS  - 31
SP  - 4961
EP  - 4969
UR  - https://hdl.handle.net/21.15107/rcub_vinar_56
ER  - 

@article{
author = "Abate, Nicola and Sallam, Hanaa S. and Rizzo, Manfredi and Nikolić, Dragana and Obradović, Milan M. and Bjelogrlic, Predrag and Isenović, Esma R.",
year = "2014",
abstract = "Resistin is an adipocyte-and monocyte-derived cytokine which has been implicated in the modulation of insulin action, energy, glucose and lipid homeostasis. Resistin has been associated with insulin resistance and many of its known complications. As a molecular link between metabolic signals, inflammation, and vascular dysfunction, resistin can be proposed as playing a significant role in the heightened inflammatory state induced by metabolic stress linked to excessive caloric intake, thus contributing to the risk for metabolic syndrome (MetS), type 2 diabetes (T2DM), and cardiovascular diseases (CVD). In this review, we highlighted the role of resistin, as an inflammatory cytokine, in the development of CVD, T2DM and the MetS.",
journal = "Current Pharmaceutical Design",
title = "Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome",
volume = "20",
number = "31",
pages = "4961-4969",
url = "https://hdl.handle.net/21.15107/rcub_vinar_56"
}

Abate, N., Sallam, H. S., Rizzo, M., Nikolić, D., Obradović, M. M., Bjelogrlic, P.,& Isenović, E. R.. (2014). Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome. in Current Pharmaceutical Design, 20(31), 4961-4969.
https://hdl.handle.net/21.15107/rcub_vinar_56

Abate N, Sallam HS, Rizzo M, Nikolić D, Obradović MM, Bjelogrlic P, Isenović ER. Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome. in Current Pharmaceutical Design. 2014;20(31):4961-4969.
https://hdl.handle.net/21.15107/rcub_vinar_56 .

Abate, Nicola, Sallam, Hanaa S., Rizzo, Manfredi, Nikolić, Dragana, Obradović, Milan M., Bjelogrlic, Predrag, Isenović, Esma R., "Resistin: An Inflammatory Cytokine. Role in Cardiovascular Diseases, Diabetes and the Metabolic Syndrome" in Current Pharmaceutical Design, 20, no. 31 (2014):4961-4969,
https://hdl.handle.net/21.15107/rcub_vinar_56 .

TY  - JOUR
AU  - Rizzo, Manfredi
AU  - Obradović, Milan M.
AU  - Labudović-Borović, Milica
AU  - Nikolić, Dragana
AU  - Montalto, Giuseppe
AU  - Rizvi, Ali A.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/290
AB  - In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.
T2  - Current Vascular Pharmacology
T1  - Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome
VL  - 12
IS  - 4
SP  - 572
EP  - 585
DO  - 10.2174/1570161111999131205160756
ER  - 

@article{
author = "Rizzo, Manfredi and Obradović, Milan M. and Labudović-Borović, Milica and Nikolić, Dragana and Montalto, Giuseppe and Rizvi, Ali A. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2014",
abstract = "In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.",
journal = "Current Vascular Pharmacology",
title = "Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome",
volume = "12",
number = "4",
pages = "572-585",
doi = "10.2174/1570161111999131205160756"
}

Rizzo, M., Obradović, M. M., Labudović-Borović, M., Nikolić, D., Montalto, G., Rizvi, A. A., Mikhailidis, D. P.,& Isenović, E. R.. (2014). Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome. in Current Vascular Pharmacology, 12(4), 572-585.
https://doi.org/10.2174/1570161111999131205160756

Rizzo M, Obradović MM, Labudović-Borović M, Nikolić D, Montalto G, Rizvi AA, Mikhailidis DP, Isenović ER. Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome. in Current Vascular Pharmacology. 2014;12(4):572-585.
doi:10.2174/1570161111999131205160756 .

Rizzo, Manfredi, Obradović, Milan M., Labudović-Borović, Milica, Nikolić, Dragana, Montalto, Giuseppe, Rizvi, Ali A., Mikhailidis, Dimitri P., Isenović, Esma R., "Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome" in Current Vascular Pharmacology, 12, no. 4 (2014):572-585,
https://doi.org/10.2174/1570161111999131205160756 . .

TY  - JOUR
AU  - Nikolić, Dragana
AU  - Katsiki, Niki
AU  - Montalto, Giuseppe
AU  - Isenović, Esma R.
AU  - Mikhailidis, Dimitri P.
AU  - Rizzo, Manfredi
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5380
AB  - Small, dense low density lipoprotein (sdLDL) represents an emerging cardiovascular risk factor, since these particles can be associated with cardiovascular disease (CVD) independently of established risk factors, including plasma lipids. Obese subjects frequently have atherogenic dyslipidaemia, including elevated sdLDL levels, in addition to elevated triglycerides (TG), very low density lipoprotein (VLDL) and apolipoprotein-B, as well as decreased high density lipoprotein cholesterol (HDL-C) levels. Obesity-related co-morbidities, such as metabolic syndrome (MetS) are also characterized by dyslipidaemia. Therefore, agents that favourably modulate LDL subclasses may be of clinical value in these subjects. Statins are the lipid-lowering drug of choice. Also, anti-obesity and lipid lowering drugs other than statins could be useful in these patients. However, the effects of anti-obesity drugs on CVD risk factors remain unclear. We review the clinical significance of sdLDL in being overweight and obesity, as well as the efficacy of anti-obesity drugs on LDL subfractions in these individuals; a short comment on HDL subclasses is also included. Our literature search was based on PubMed and Scopus listings. Further research is required to fully explore both the significance of sdLDL and the efficacy of anti-obesity drugs on LDL subfractions in being overweight, obesity and MetS. Improving the lipoprotein profile in these patients may represent an efficient approach for reducing cardiovascular risk.
T2  - Nutrients
T1  - Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches
VL  - 5
IS  - 3
SP  - 928
EP  - 948
DO  - 10.3390/nu5030928
ER  - 

@article{
author = "Nikolić, Dragana and Katsiki, Niki and Montalto, Giuseppe and Isenović, Esma R. and Mikhailidis, Dimitri P. and Rizzo, Manfredi",
year = "2013",
abstract = "Small, dense low density lipoprotein (sdLDL) represents an emerging cardiovascular risk factor, since these particles can be associated with cardiovascular disease (CVD) independently of established risk factors, including plasma lipids. Obese subjects frequently have atherogenic dyslipidaemia, including elevated sdLDL levels, in addition to elevated triglycerides (TG), very low density lipoprotein (VLDL) and apolipoprotein-B, as well as decreased high density lipoprotein cholesterol (HDL-C) levels. Obesity-related co-morbidities, such as metabolic syndrome (MetS) are also characterized by dyslipidaemia. Therefore, agents that favourably modulate LDL subclasses may be of clinical value in these subjects. Statins are the lipid-lowering drug of choice. Also, anti-obesity and lipid lowering drugs other than statins could be useful in these patients. However, the effects of anti-obesity drugs on CVD risk factors remain unclear. We review the clinical significance of sdLDL in being overweight and obesity, as well as the efficacy of anti-obesity drugs on LDL subfractions in these individuals; a short comment on HDL subclasses is also included. Our literature search was based on PubMed and Scopus listings. Further research is required to fully explore both the significance of sdLDL and the efficacy of anti-obesity drugs on LDL subfractions in being overweight, obesity and MetS. Improving the lipoprotein profile in these patients may represent an efficient approach for reducing cardiovascular risk.",
journal = "Nutrients",
title = "Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches",
volume = "5",
number = "3",
pages = "928-948",
doi = "10.3390/nu5030928"
}

Nikolić, D., Katsiki, N., Montalto, G., Isenović, E. R., Mikhailidis, D. P.,& Rizzo, M.. (2013). Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches. in Nutrients, 5(3), 928-948.
https://doi.org/10.3390/nu5030928

Nikolić D, Katsiki N, Montalto G, Isenović ER, Mikhailidis DP, Rizzo M. Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches. in Nutrients. 2013;5(3):928-948.
doi:10.3390/nu5030928 .

Nikolić, Dragana, Katsiki, Niki, Montalto, Giuseppe, Isenović, Esma R., Mikhailidis, Dimitri P., Rizzo, Manfredi, "Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches" in Nutrients, 5, no. 3 (2013):928-948,
https://doi.org/10.3390/nu5030928 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Bjelogrlic, Predrag
AU  - Rizzo, Manfredi
AU  - Katsiki, Niki
AU  - Haidara, Mohamed A.
AU  - Stewart, Alan J.
AU  - Jovanović, Aleksandra
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5672
AB  - Obesity is associated with aberrant sodium/potassium-ATPase (Na+/K+-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of Na+/K+-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in Na+/K+-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of Na+/K+-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on Na+/K+-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on Na+/K+-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate Na+/K+-ATPase activity.
T2  - Journal of Endocrinology
T1  - Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases
VL  - 218
IS  - 3
SP  - R13
EP  - R23
DO  - 10.1530/JOE-13-0144
ER  - 

@article{
author = "Obradović, Milan M. and Bjelogrlic, Predrag and Rizzo, Manfredi and Katsiki, Niki and Haidara, Mohamed A. and Stewart, Alan J. and Jovanović, Aleksandra and Isenović, Esma R.",
year = "2013",
abstract = "Obesity is associated with aberrant sodium/potassium-ATPase (Na+/K+-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of Na+/K+-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in Na+/K+-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of Na+/K+-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on Na+/K+-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on Na+/K+-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate Na+/K+-ATPase activity.",
journal = "Journal of Endocrinology",
title = "Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases",
volume = "218",
number = "3",
pages = "R13-R23",
doi = "10.1530/JOE-13-0144"
}

Obradović, M. M., Bjelogrlic, P., Rizzo, M., Katsiki, N., Haidara, M. A., Stewart, A. J., Jovanović, A.,& Isenović, E. R.. (2013). Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases. in Journal of Endocrinology, 218(3), R13-R23.
https://doi.org/10.1530/JOE-13-0144

Obradović MM, Bjelogrlic P, Rizzo M, Katsiki N, Haidara MA, Stewart AJ, Jovanović A, Isenović ER. Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases. in Journal of Endocrinology. 2013;218(3):R13-R23.
doi:10.1530/JOE-13-0144 .

Obradović, Milan M., Bjelogrlic, Predrag, Rizzo, Manfredi, Katsiki, Niki, Haidara, Mohamed A., Stewart, Alan J., Jovanović, Aleksandra, Isenović, Esma R., "Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases" in Journal of Endocrinology, 218, no. 3 (2013):R13-R23,
https://doi.org/10.1530/JOE-13-0144 . .

TY  - JOUR
AU  - Resanović, Ivana
AU  - Rizzo, Manfredi
AU  - Zafirović, Sonja
AU  - Bjelogrlic, P.
AU  - Perović, Milan
AU  - Savić, K.
AU  - Patti, A. M.
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5680
AB  - Estrogens are secreted primarily by the ovaries and placenta, by the testes in men and also produced by peripheral steroidogenic conversion. The 3 major naturally occurring estrogens are: 17 beta-estradiol (E-2), estrone and estriol, of which E-2 is the predominant and most active. The actions of E-2 are mediated by at least 3 different receptors - the classical ERs (ER alpha and ER beta) and G-protein coupled receptor 30 (GPR30). E-2 signaling in cardiomyocytes involves ER alpha- and ER beta-independent pathways, and treatment with the E-2 receptor antagonists (Selective Estrogen Receptor Modulators- SERMs), which are agonists of GPR30, inhibits cardiac cell growth. Effects of E-2 in preventing endothelial dysfunction, a prerequisite of atherosclerosis, are well recognized. Atherosclerosis involves interaction between the cells of the arterial wall endothelial cells (EC) and vascular smooth muscle cell (VSMC), as well as migration of macrophages into wall tunica media. It is predominantly developed at sites with abnormally high shear stress, such as bifurcations or branching of arteries, initiated by an injury to the endothelium and exposure to atherogenic lipids and toxins, such as those contained in tobacco smoke or infectious agents. Animal studies have shown effects of E-2 in preventing atherosclerosis, inflammation and endothelial or vascular dysfunction. Gender differences along this pathogenic pathway have been also described. We review the data from the available animal and human studies, which focus on anti-atherogenic effects of E-2. These studies represent evidence, albeit indirect, for an inhibitory effect of E-2 on the progression of coronary artery atherosclerosis.
T2  - Hormone and Metabolic Research
T1  - Anti-atherogenic Effects of 17 beta-Estradiol
VL  - 45
IS  - 10
SP  - 701
EP  - 708
DO  - 10.1055/s-0033-1343478
ER  - 

@article{
author = "Resanović, Ivana and Rizzo, Manfredi and Zafirović, Sonja and Bjelogrlic, P. and Perović, Milan and Savić, K. and Patti, A. M. and Isenović, Esma R.",
year = "2013",
abstract = "Estrogens are secreted primarily by the ovaries and placenta, by the testes in men and also produced by peripheral steroidogenic conversion. The 3 major naturally occurring estrogens are: 17 beta-estradiol (E-2), estrone and estriol, of which E-2 is the predominant and most active. The actions of E-2 are mediated by at least 3 different receptors - the classical ERs (ER alpha and ER beta) and G-protein coupled receptor 30 (GPR30). E-2 signaling in cardiomyocytes involves ER alpha- and ER beta-independent pathways, and treatment with the E-2 receptor antagonists (Selective Estrogen Receptor Modulators- SERMs), which are agonists of GPR30, inhibits cardiac cell growth. Effects of E-2 in preventing endothelial dysfunction, a prerequisite of atherosclerosis, are well recognized. Atherosclerosis involves interaction between the cells of the arterial wall endothelial cells (EC) and vascular smooth muscle cell (VSMC), as well as migration of macrophages into wall tunica media. It is predominantly developed at sites with abnormally high shear stress, such as bifurcations or branching of arteries, initiated by an injury to the endothelium and exposure to atherogenic lipids and toxins, such as those contained in tobacco smoke or infectious agents. Animal studies have shown effects of E-2 in preventing atherosclerosis, inflammation and endothelial or vascular dysfunction. Gender differences along this pathogenic pathway have been also described. We review the data from the available animal and human studies, which focus on anti-atherogenic effects of E-2. These studies represent evidence, albeit indirect, for an inhibitory effect of E-2 on the progression of coronary artery atherosclerosis.",
journal = "Hormone and Metabolic Research",
title = "Anti-atherogenic Effects of 17 beta-Estradiol",
volume = "45",
number = "10",
pages = "701-708",
doi = "10.1055/s-0033-1343478"
}

Resanović, I., Rizzo, M., Zafirović, S., Bjelogrlic, P., Perović, M., Savić, K., Patti, A. M.,& Isenović, E. R.. (2013). Anti-atherogenic Effects of 17 beta-Estradiol. in Hormone and Metabolic Research, 45(10), 701-708.
https://doi.org/10.1055/s-0033-1343478

Resanović I, Rizzo M, Zafirović S, Bjelogrlic P, Perović M, Savić K, Patti AM, Isenović ER. Anti-atherogenic Effects of 17 beta-Estradiol. in Hormone and Metabolic Research. 2013;45(10):701-708.
doi:10.1055/s-0033-1343478 .

Resanović, Ivana, Rizzo, Manfredi, Zafirović, Sonja, Bjelogrlic, P., Perović, Milan, Savić, K., Patti, A. M., Isenović, Esma R., "Anti-atherogenic Effects of 17 beta-Estradiol" in Hormone and Metabolic Research, 45, no. 10 (2013):701-708,
https://doi.org/10.1055/s-0033-1343478 . .

TY  - JOUR
AU  - Banach, Maciej
AU  - Rizzo, Manfredi
AU  - Obradović, Milan M.
AU  - Montalto, Giuseppe
AU  - Rysz, Jacek
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5502
AB  - Plasma low-density lipoprotein cholesterol (LDL-C) is one of the biomarkers of cardiovascular disease (CVD) risk. LDL is cleared from the circulation preferentially through the LDL receptor (LDLR) pathway. Proprotein convertase subtilisin/kexin 9 (PCSK9) promotes the degradation of the LDLR. PCSK9 inhibition is attractive as a new strategy for lowering LDL-C levels, especially in combination with lipid lowering drugs such as statins. We review data from the available studies which focus on PCSK9 as a potential target in the treatment of hyperlipidemia. Further studies are still necessary to investigate the potential underlying mechanisms involved.
T2  - Current Pharmaceutical Design
T1  - PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?
VL  - 19
IS  - 21
SP  - 3869
EP  - 3877
DO  - 10.2174/13816128113199990303
ER  - 

@article{
author = "Banach, Maciej and Rizzo, Manfredi and Obradović, Milan M. and Montalto, Giuseppe and Rysz, Jacek and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2013",
abstract = "Plasma low-density lipoprotein cholesterol (LDL-C) is one of the biomarkers of cardiovascular disease (CVD) risk. LDL is cleared from the circulation preferentially through the LDL receptor (LDLR) pathway. Proprotein convertase subtilisin/kexin 9 (PCSK9) promotes the degradation of the LDLR. PCSK9 inhibition is attractive as a new strategy for lowering LDL-C levels, especially in combination with lipid lowering drugs such as statins. We review data from the available studies which focus on PCSK9 as a potential target in the treatment of hyperlipidemia. Further studies are still necessary to investigate the potential underlying mechanisms involved.",
journal = "Current Pharmaceutical Design",
title = "PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?",
volume = "19",
number = "21",
pages = "3869-3877",
doi = "10.2174/13816128113199990303"
}

Banach, M., Rizzo, M., Obradović, M. M., Montalto, G., Rysz, J., Mikhailidis, D. P.,& Isenović, E. R.. (2013). PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?. in Current Pharmaceutical Design, 19(21), 3869-3877.
https://doi.org/10.2174/13816128113199990303

Banach M, Rizzo M, Obradović MM, Montalto G, Rysz J, Mikhailidis DP, Isenović ER. PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?. in Current Pharmaceutical Design. 2013;19(21):3869-3877.
doi:10.2174/13816128113199990303 .

Banach, Maciej, Rizzo, Manfredi, Obradović, Milan M., Montalto, Giuseppe, Rysz, Jacek, Mikhailidis, Dimitri P., Isenović, Esma R., "PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?" in Current Pharmaceutical Design, 19, no. 21 (2013):3869-3877,
https://doi.org/10.2174/13816128113199990303 . .

TY  - JOUR
AU  - Rizzo, Manfredi
AU  - Rizvi, Ali A.
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Obradović, Milan M.
AU  - Montalto, Giuseppe
AU  - Boutjdir, Mohamed
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5565
AB  - Ghrelin is a peptide hormone produced mainly in the stomach that has widespread tissue distribution and diverse hormonal, metabolic and cardiovascular activities. The circulating ghrelin concentration increases during fasting and decreases after food intake. Ghrelin secretion may thus be initiated by food intake and is possibly controlled by nutritional factors. Lean subjects have increased levels of circulating ghrelin compared with obese subjects. Recent reports show that low plasma ghrelin is associated with elevated fasting insulin levels, insulin resistance and type 2 diabetes mellitus. Factors involved in the regulation of ghrelin secretion have not yet been defined; however, it is assumed that blood glucose levels represent a significant regulator. Recent evidence indicates that ghrelin can increase myocardial contractility, enhance vasodilatation, and has protective effect from myocardial damage. It has been shown that ghrelin may improve cardiac function through growth hormone (GH)-dependent mechanisms but there is also evidence to suggest that ghrelins cardioprotective activity is independent of GH. Recent data demonstrate that ghrelin can influence key events in atherogenesis. Thus, ghrelin may be a new target for the treatment of some cardiovascular diseases. In this review, we consider the current literature focusing on ghrelin as a potential antiatherogenic agent in the treatment of various pathophysiological conditions.
T2  - Current Pharmaceutical Design
T1  - A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin
VL  - 19
IS  - 27
SP  - 4953
EP  - 4963
DO  - 10.2174/1381612811319270018
ER  - 

@article{
author = "Rizzo, Manfredi and Rizvi, Ali A. and Sudar, Emina and Soskić, Sanja S. and Obradović, Milan M. and Montalto, Giuseppe and Boutjdir, Mohamed and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2013",
abstract = "Ghrelin is a peptide hormone produced mainly in the stomach that has widespread tissue distribution and diverse hormonal, metabolic and cardiovascular activities. The circulating ghrelin concentration increases during fasting and decreases after food intake. Ghrelin secretion may thus be initiated by food intake and is possibly controlled by nutritional factors. Lean subjects have increased levels of circulating ghrelin compared with obese subjects. Recent reports show that low plasma ghrelin is associated with elevated fasting insulin levels, insulin resistance and type 2 diabetes mellitus. Factors involved in the regulation of ghrelin secretion have not yet been defined; however, it is assumed that blood glucose levels represent a significant regulator. Recent evidence indicates that ghrelin can increase myocardial contractility, enhance vasodilatation, and has protective effect from myocardial damage. It has been shown that ghrelin may improve cardiac function through growth hormone (GH)-dependent mechanisms but there is also evidence to suggest that ghrelins cardioprotective activity is independent of GH. Recent data demonstrate that ghrelin can influence key events in atherogenesis. Thus, ghrelin may be a new target for the treatment of some cardiovascular diseases. In this review, we consider the current literature focusing on ghrelin as a potential antiatherogenic agent in the treatment of various pathophysiological conditions.",
journal = "Current Pharmaceutical Design",
title = "A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin",
volume = "19",
number = "27",
pages = "4953-4963",
doi = "10.2174/1381612811319270018"
}

Rizzo, M., Rizvi, A. A., Sudar, E., Soskić, S. S., Obradović, M. M., Montalto, G., Boutjdir, M., Mikhailidis, D. P.,& Isenović, E. R.. (2013). A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin. in Current Pharmaceutical Design, 19(27), 4953-4963.
https://doi.org/10.2174/1381612811319270018

Rizzo M, Rizvi AA, Sudar E, Soskić SS, Obradović MM, Montalto G, Boutjdir M, Mikhailidis DP, Isenović ER. A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin. in Current Pharmaceutical Design. 2013;19(27):4953-4963.
doi:10.2174/1381612811319270018 .

Rizzo, Manfredi, Rizvi, Ali A., Sudar, Emina, Soskić, Sanja S., Obradović, Milan M., Montalto, Giuseppe, Boutjdir, Mohamed, Mikhailidis, Dimitri P., Isenović, Esma R., "A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin" in Current Pharmaceutical Design, 19, no. 27 (2013):4953-4963,
https://doi.org/10.2174/1381612811319270018 . .

TY  - CHAP
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Zarić, Božidarka
AU  - Rašić-Milutinović, Zorica
AU  - Smiljanić, Katarina
AU  - Radak, Đorđe J.
AU  - Mikhailidis, Dimitri P.
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8685
AB  - Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.
T2  - Ghrelin: Production, Action Mechanisms and Physiological Effects
T1  - Ghrelin, obesity and atherosclerosis
SP  - 111
EP  - 126
UR  - https://hdl.handle.net/21.15107/rcub_vinar_8685
ER  - 

@inbook{
author = "Sudar, Emina and Soskić, Sanja S. and Zarić, Božidarka and Rašić-Milutinović, Zorica and Smiljanić, Katarina and Radak, Đorđe J. and Mikhailidis, Dimitri P. and Rizzo, Manfredi and Isenović, Esma R.",
year = "2012",
abstract = "Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.",
journal = "Ghrelin: Production, Action Mechanisms and Physiological Effects",
booktitle = "Ghrelin, obesity and atherosclerosis",
pages = "111-126",
url = "https://hdl.handle.net/21.15107/rcub_vinar_8685"
}

Sudar, E., Soskić, S. S., Zarić, B., Rašić-Milutinović, Z., Smiljanić, K., Radak, Đ. J., Mikhailidis, D. P., Rizzo, M.,& Isenović, E. R.. (2012). Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects, 111-126.
https://hdl.handle.net/21.15107/rcub_vinar_8685

Sudar E, Soskić SS, Zarić B, Rašić-Milutinović Z, Smiljanić K, Radak ĐJ, Mikhailidis DP, Rizzo M, Isenović ER. Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects. 2012;:111-126.
https://hdl.handle.net/21.15107/rcub_vinar_8685 .

Sudar, Emina, Soskić, Sanja S., Zarić, Božidarka, Rašić-Milutinović, Zorica, Smiljanić, Katarina, Radak, Đorđe J., Mikhailidis, Dimitri P., Rizzo, Manfredi, Isenović, Esma R., "Ghrelin, obesity and atherosclerosis" in Ghrelin: Production, Action Mechanisms and Physiological Effects (2012):111-126,
https://hdl.handle.net/21.15107/rcub_vinar_8685 .

TY  - JOUR
AU  - Haidara, Mohamed A.
AU  - Mikhailidis, Dimitri P.
AU  - Yassin, Hanaa Z.
AU  - Dobutović, Branislava
AU  - Smiljanić, Katarina
AU  - Soskić, Sanja S.
AU  - Mousa, Shaker A.
AU  - Rizzo, Manfredi
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4662
AB  - The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.
T2  - Current Pharmaceutical Design
T1  - Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome
VL  - 17
IS  - 33
SP  - 3699
EP  - 3712
DO  - 10.2174/138161211798220882
ER  - 

@article{
author = "Haidara, Mohamed A. and Mikhailidis, Dimitri P. and Yassin, Hanaa Z. and Dobutović, Branislava and Smiljanić, Katarina and Soskić, Sanja S. and Mousa, Shaker A. and Rizzo, Manfredi and Isenović, Esma R.",
year = "2011",
abstract = "The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.",
journal = "Current Pharmaceutical Design",
title = "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome",
volume = "17",
number = "33",
pages = "3699-3712",
doi = "10.2174/138161211798220882"
}

Haidara, M. A., Mikhailidis, D. P., Yassin, H. Z., Dobutović, B., Smiljanić, K., Soskić, S. S., Mousa, S. A., Rizzo, M.,& Isenović, E. R.. (2011). Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design, 17(33), 3699-3712.
https://doi.org/10.2174/138161211798220882

Haidara MA, Mikhailidis DP, Yassin HZ, Dobutović B, Smiljanić K, Soskić SS, Mousa SA, Rizzo M, Isenović ER. Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design. 2011;17(33):3699-3712.
doi:10.2174/138161211798220882 .

Haidara, Mohamed A., Mikhailidis, Dimitri P., Yassin, Hanaa Z., Dobutović, Branislava, Smiljanić, Katarina, Soskić, Sanja S., Mousa, Shaker A., Rizzo, Manfredi, Isenović, Esma R., "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome" in Current Pharmaceutical Design, 17, no. 33 (2011):3699-3712,
https://doi.org/10.2174/138161211798220882 . .