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Banach, Maciej

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  • Banach, Maciej (3)
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Author's Bibliography

Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications

Zarić, Božidarka; Obradović, Milan M.; Trpković, Andreja; Banach, Maciej; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2020)

TY  - JOUR
AU  - Zarić, Božidarka
AU  - Obradović, Milan M.
AU  - Trpković, Andreja
AU  - Banach, Maciej
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8811
AB  - The endothelium consists of a monolayer of Endothelial Cells (ECs) which form the inner cellular lining of veins, arteries, capillaries and lymphatic vessels. ECs interact with the blood and lymph. The endothelium fulfils functions such as vasodilatation, regulation of adhesion, infiltration of leukocytes, inhibition of platelet adhesion, vessel remodeling and lipoprotein metabolism. ECs synthesize and release compounds such as Nitric Oxide (NO), metabolites of arachidonic acid, Reactive Oxygen Species (ROS) and enzymes that degrade the extracellular matrix. Endothelial dysfunction represents a phenotype prone to atherogenesis and may be used as a marker of atherosclerotic risk. Such dysfunction includes impaired synthesis and availability of NO and an imbalance in the relative contribution of endothelial-derived relaxing factors and contracting factors such as endothelin-1 and angiotensin. This dysfunction appears before the earliest anatomic evidence of atherosclerosis and could be an important initial step in further development of atherosclerosis. Endothelial dysfunction was historically treated with vitamin C supplementation and L-arginine supplementation. Short term improvement of the expression of adhesion molecule and endothelial function during antioxidant therapy has been observed. Statins are used in the treatment of hyperlipidaemia, a risk factor for cardiovascular disease. Future studies should focus on identifying the mechanisms involved in the beneficial effects of statins on the endothelium. This may help develop drugs specifically aimed at endothelial dysfunction. © 2020 Bentham Science Publishers.
T2  - Current Medicinal Chemistry
T1  - Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications
VL  - 27
IS  - 7
SP  - 1021
EP  - 1040
DO  - 10.2174/0929867326666190903112146
ER  - 
@article{
author = "Zarić, Božidarka and Obradović, Milan M. and Trpković, Andreja and Banach, Maciej and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2020",
url = "https://vinar.vin.bg.ac.rs/handle/123456789/8811",
abstract = "The endothelium consists of a monolayer of Endothelial Cells (ECs) which form the inner cellular lining of veins, arteries, capillaries and lymphatic vessels. ECs interact with the blood and lymph. The endothelium fulfils functions such as vasodilatation, regulation of adhesion, infiltration of leukocytes, inhibition of platelet adhesion, vessel remodeling and lipoprotein metabolism. ECs synthesize and release compounds such as Nitric Oxide (NO), metabolites of arachidonic acid, Reactive Oxygen Species (ROS) and enzymes that degrade the extracellular matrix. Endothelial dysfunction represents a phenotype prone to atherogenesis and may be used as a marker of atherosclerotic risk. Such dysfunction includes impaired synthesis and availability of NO and an imbalance in the relative contribution of endothelial-derived relaxing factors and contracting factors such as endothelin-1 and angiotensin. This dysfunction appears before the earliest anatomic evidence of atherosclerosis and could be an important initial step in further development of atherosclerosis. Endothelial dysfunction was historically treated with vitamin C supplementation and L-arginine supplementation. Short term improvement of the expression of adhesion molecule and endothelial function during antioxidant therapy has been observed. Statins are used in the treatment of hyperlipidaemia, a risk factor for cardiovascular disease. Future studies should focus on identifying the mechanisms involved in the beneficial effects of statins on the endothelium. This may help develop drugs specifically aimed at endothelial dysfunction. © 2020 Bentham Science Publishers.",
journal = "Current Medicinal Chemistry",
title = "Endothelial dysfunction in dyslipidaemia: Molecular mechanisms and clinical implications",
volume = "27",
number = "7",
pages = "1021-1040",
doi = "10.2174/0929867326666190903112146"
}
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Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study

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

(2015)

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  - http://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",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/508",
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"
}
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59

PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?

Banach, Maciej; Rizzo, Manfredi; Obradović, Milan M.; Montalto, Giuseppe; Rysz, Jacek; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2013)

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  - http://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",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5502",
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"
}
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