TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Katsiki, Niki
AU  - Resanović, Ivana
AU  - Jovanović, Aleksandra
AU  - Sudar, Emina
AU  - Zafirović, Sonja
AU  - Mousa, Shaker A.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1521
AB  - Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.
T2  - Current Vascular Pharmacology
T1  - Apoptosis and Acute Brain Ischemia in Ischemic Stroke
VL  - 15
IS  - 2
SP  - 115
EP  - 122
DO  - 10.2174/1570161115666161104095522
ER  - 

@article{
author = "Radak, Đorđe J. and Katsiki, Niki and Resanović, Ivana and Jovanović, Aleksandra and Sudar, Emina and Zafirović, Sonja and Mousa, Shaker A. and Isenović, Esma R.",
year = "2017",
abstract = "Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.",
journal = "Current Vascular Pharmacology",
title = "Apoptosis and Acute Brain Ischemia in Ischemic Stroke",
volume = "15",
number = "2",
pages = "115-122",
doi = "10.2174/1570161115666161104095522"
}

Radak, Đ. J., Katsiki, N., Resanović, I., Jovanović, A., Sudar, E., Zafirović, S., Mousa, S. A.,& Isenović, E. R.. (2017). Apoptosis and Acute Brain Ischemia in Ischemic Stroke. in Current Vascular Pharmacology, 15(2), 115-122.
https://doi.org/10.2174/1570161115666161104095522

Radak ĐJ, Katsiki N, Resanović I, Jovanović A, Sudar E, Zafirović S, Mousa SA, Isenović ER. Apoptosis and Acute Brain Ischemia in Ischemic Stroke. in Current Vascular Pharmacology. 2017;15(2):115-122.
doi:10.2174/1570161115666161104095522 .

Radak, Đorđe J., Katsiki, Niki, Resanović, Ivana, Jovanović, Aleksandra, Sudar, Emina, Zafirović, Sonja, Mousa, Shaker A., Isenović, Esma R., "Apoptosis and Acute Brain Ischemia in Ischemic Stroke" in Current Vascular Pharmacology, 15, no. 2 (2017):115-122,
https://doi.org/10.2174/1570161115666161104095522 . .

TY  - JOUR
AU  - Ilinčić, Branislava
AU  - Stokić, Edita
AU  - Stošić, Zoran
AU  - Kojić, Nevena Eremic
AU  - Katsiki, Niki
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1371
AB  - Introduction: Obesity and inadequate vitamin D status are associated with endothelial dysfunction and cardiovascular disease. We evaluated the associations between vitamin D status (i.e. serum levels of 25-hydroxyvitamin D (25(OH)D)), biomarkers of endothelial dysfunction (i.e. serum concentrations of soluble intercellular adhesion molecule 1 (sICAM-1) and soluble E-selectin (sE-selectin)), inflammatory markers (i.e. high-sensitivity C-reactive protein (hsCRP) and fibrinogen) and cardiometabolic risk factors. Material and methods: Fifty obese (body mass index (BMI) GT = 30 kg/m(2)) non-diabetic adults (mean age: 36.2 +/- 5.4 years) without pre-existing cardiovascular abnormalities and 25 clinically healthy, normal weight and age matched individuals were included. Anthropometric parameters, markers of glucose and lipid metabolism, and serum levels of inflammatory and endothelial dysfunction biomarkers were assessed in all subjects. Results: The mean serum 25(OH)D level was significantly lower in the obese group than in controls (33.5 +/- 15.2 vs. 60.1 +/- 23.1 nmol/l; p LT 0.001). In the obese group, sE-selectin (36.4 (32.1-47.2) vs. 32.4 (24.6-35.5) ng/ml, p LT 0.05) and hsCRP (6.0 +/- 3.4 vs. 3.5 1.0 mg/l, p LT 0.05) were significantly higher in individuals with lower than median vitamin D levels (i.e. 31 nmol/l) compared with those with higher vitamin D levels. In multivariable linear regression analysis, hsCRP (beta = 0.43; p LT 0.001) and sE-selectin (beta = 0.30; p = 0.03) were independently and significantly associated with serum 25(OH)D levels in the obese group. Conclusions: Vitamin D levels may be related to increased levels of biomarkers of endothelial dysfunction and inflammation in obese non-diabetic individuals.
T2  - Archives of Medical Science
T1  - Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study
VL  - 13
IS  - 1
SP  - 53
EP  - 60
DO  - 10.5114/aoms.2016.61812
ER  - 

@article{
author = "Ilinčić, Branislava and Stokić, Edita and Stošić, Zoran and Kojić, Nevena Eremic and Katsiki, Niki and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2017",
abstract = "Introduction: Obesity and inadequate vitamin D status are associated with endothelial dysfunction and cardiovascular disease. We evaluated the associations between vitamin D status (i.e. serum levels of 25-hydroxyvitamin D (25(OH)D)), biomarkers of endothelial dysfunction (i.e. serum concentrations of soluble intercellular adhesion molecule 1 (sICAM-1) and soluble E-selectin (sE-selectin)), inflammatory markers (i.e. high-sensitivity C-reactive protein (hsCRP) and fibrinogen) and cardiometabolic risk factors. Material and methods: Fifty obese (body mass index (BMI) GT = 30 kg/m(2)) non-diabetic adults (mean age: 36.2 +/- 5.4 years) without pre-existing cardiovascular abnormalities and 25 clinically healthy, normal weight and age matched individuals were included. Anthropometric parameters, markers of glucose and lipid metabolism, and serum levels of inflammatory and endothelial dysfunction biomarkers were assessed in all subjects. Results: The mean serum 25(OH)D level was significantly lower in the obese group than in controls (33.5 +/- 15.2 vs. 60.1 +/- 23.1 nmol/l; p LT 0.001). In the obese group, sE-selectin (36.4 (32.1-47.2) vs. 32.4 (24.6-35.5) ng/ml, p LT 0.05) and hsCRP (6.0 +/- 3.4 vs. 3.5 1.0 mg/l, p LT 0.05) were significantly higher in individuals with lower than median vitamin D levels (i.e. 31 nmol/l) compared with those with higher vitamin D levels. In multivariable linear regression analysis, hsCRP (beta = 0.43; p LT 0.001) and sE-selectin (beta = 0.30; p = 0.03) were independently and significantly associated with serum 25(OH)D levels in the obese group. Conclusions: Vitamin D levels may be related to increased levels of biomarkers of endothelial dysfunction and inflammation in obese non-diabetic individuals.",
journal = "Archives of Medical Science",
title = "Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study",
volume = "13",
number = "1",
pages = "53-60",
doi = "10.5114/aoms.2016.61812"
}

Ilinčić, B., Stokić, E., Stošić, Z., Kojić, N. E., Katsiki, N., Mikhailidis, D. P.,& Isenović, E. R.. (2017). Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study. in Archives of Medical Science, 13(1), 53-60.
https://doi.org/10.5114/aoms.2016.61812

Ilinčić B, Stokić E, Stošić Z, Kojić NE, Katsiki N, Mikhailidis DP, Isenović ER. Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study. in Archives of Medical Science. 2017;13(1):53-60.
doi:10.5114/aoms.2016.61812 .

Ilinčić, Branislava, Stokić, Edita, Stošić, Zoran, Kojić, Nevena Eremic, Katsiki, Niki, Mikhailidis, Dimitri P., Isenović, Esma R., "Vitamin D status and circulating biomarkers of endothelial dysfunction and inflammation in non-diabetic obese individuals: a pilot study" in Archives of Medical Science, 13, no. 1 (2017):53-60,
https://doi.org/10.5114/aoms.2016.61812 . .

TY  - JOUR
AU  - Radak, Đorđe J.
AU  - Tanasković, Slobodan
AU  - Katsiki, Niki
AU  - Isenović, Esma R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1005
AB  - An inverse association between diabetes mellitus (DM) and abdominal aortic aneurysm (AAA) risk have been reported. Apart from a lower AAA prevalence among patients with vs without DM, there are data showing that DM may exert a protective role on aneurysmal growth in patients with small AAAs, thus decreasing the risk of rupture. As atherosclerosis has almost the same risk factors as aneurysms, the decreased AAA prevalence in patients with DM may indicate that atherosclerosis is an associated feature and not a cause of the aneurysms. Alternatively, DM may be associated with factors that influence AAA formation. In this narrative review, we discuss the inverse association between DM and AAA. We also comment on underlying cellular and genetic pathophysiological mechanisms of DM, AAA and atherosclerosis. The effects of drugs, commonly prescribed in DM patients, on AAA development and growth are also considered.
T2  - Current Vascular Pharmacology
T1  - Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?
VL  - 14
IS  - 2
SP  - 196
EP  - 200
DO  - 10.2174/1570161113666150529125127
ER  - 

@article{
author = "Radak, Đorđe J. and Tanasković, Slobodan and Katsiki, Niki and Isenović, Esma R.",
year = "2016",
abstract = "An inverse association between diabetes mellitus (DM) and abdominal aortic aneurysm (AAA) risk have been reported. Apart from a lower AAA prevalence among patients with vs without DM, there are data showing that DM may exert a protective role on aneurysmal growth in patients with small AAAs, thus decreasing the risk of rupture. As atherosclerosis has almost the same risk factors as aneurysms, the decreased AAA prevalence in patients with DM may indicate that atherosclerosis is an associated feature and not a cause of the aneurysms. Alternatively, DM may be associated with factors that influence AAA formation. In this narrative review, we discuss the inverse association between DM and AAA. We also comment on underlying cellular and genetic pathophysiological mechanisms of DM, AAA and atherosclerosis. The effects of drugs, commonly prescribed in DM patients, on AAA development and growth are also considered.",
journal = "Current Vascular Pharmacology",
title = "Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?",
volume = "14",
number = "2",
pages = "196-200",
doi = "10.2174/1570161113666150529125127"
}

Radak, Đ. J., Tanasković, S., Katsiki, N.,& Isenović, E. R.. (2016). Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?. in Current Vascular Pharmacology, 14(2), 196-200.
https://doi.org/10.2174/1570161113666150529125127

Radak ĐJ, Tanasković S, Katsiki N, Isenović ER. Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?. in Current Vascular Pharmacology. 2016;14(2):196-200.
doi:10.2174/1570161113666150529125127 .

Radak, Đorđe J., Tanasković, Slobodan, Katsiki, Niki, Isenović, Esma R., "Protective Role of Diabetes Mellitus on Abdominal Aortic Aneurysm Pathogenesis: Myth or Reality?" in Current Vascular Pharmacology, 14, no. 2 (2016):196-200,
https://doi.org/10.2174/1570161113666150529125127 . .

TY  - JOUR
AU  - Krdzic, Ivana
AU  - Covickovic-Sternic, Nadezda
AU  - Katsiki, Niki
AU  - Isenović, Esma R.
AU  - Radak, Đorđe J.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/516
AB  - We assessed reactivity of cerebral vessels on hypercapnia in patients with carotid occlusive disease. The effects of vascular risk factors on carotid atherosclerosis and vasomotor reactivity (VMR) of cerebral arterioles were also examined. Patients (n = 50) with carotid stenosis (30% in 1 or both sides) were included; 30 patients acted as controls. Hypertension, hyperlipidemia, diabetes, cardiac diseases, inflammation, and smoking were recorded. Vasomotor reactivity was assessed with the apnea test by transcranial Doppler ultrasonography and estimated by flow velocity changes in the middle cerebral artery before and after hypercapnia induction. Vasomotor reactivity was defined by the breath holding index, and values under 0.69 were considered critical for VMR impairment. Vasomotor reactivity reduction was significant (P = .004) in patients with severe carotid stenosis ( GT 70%) and with symptomatic carotid disease (P LT .05). The risk factors did not significantly influence VMR reduction. Severe carotid stenosis impairs VMR and may increase the risk of stroke, especially in symptomatic patients.
T2  - Angiology
T1  - Correlation of Carotid Artery Disease Severity and Vasomotor Response of Cerebral Blood Vessels
VL  - 66
IS  - 5
SP  - 481
EP  - 487
DO  - 10.1177/0003319714538312
ER  - 

@article{
author = "Krdzic, Ivana and Covickovic-Sternic, Nadezda and Katsiki, Niki and Isenović, Esma R. and Radak, Đorđe J.",
year = "2015",
abstract = "We assessed reactivity of cerebral vessels on hypercapnia in patients with carotid occlusive disease. The effects of vascular risk factors on carotid atherosclerosis and vasomotor reactivity (VMR) of cerebral arterioles were also examined. Patients (n = 50) with carotid stenosis (30% in 1 or both sides) were included; 30 patients acted as controls. Hypertension, hyperlipidemia, diabetes, cardiac diseases, inflammation, and smoking were recorded. Vasomotor reactivity was assessed with the apnea test by transcranial Doppler ultrasonography and estimated by flow velocity changes in the middle cerebral artery before and after hypercapnia induction. Vasomotor reactivity was defined by the breath holding index, and values under 0.69 were considered critical for VMR impairment. Vasomotor reactivity reduction was significant (P = .004) in patients with severe carotid stenosis ( GT 70%) and with symptomatic carotid disease (P LT .05). The risk factors did not significantly influence VMR reduction. Severe carotid stenosis impairs VMR and may increase the risk of stroke, especially in symptomatic patients.",
journal = "Angiology",
title = "Correlation of Carotid Artery Disease Severity and Vasomotor Response of Cerebral Blood Vessels",
volume = "66",
number = "5",
pages = "481-487",
doi = "10.1177/0003319714538312"
}

Krdzic, I., Covickovic-Sternic, N., Katsiki, N., Isenović, E. R.,& Radak, Đ. J.. (2015). Correlation of Carotid Artery Disease Severity and Vasomotor Response of Cerebral Blood Vessels. in Angiology, 66(5), 481-487.
https://doi.org/10.1177/0003319714538312

Krdzic I, Covickovic-Sternic N, Katsiki N, Isenović ER, Radak ĐJ. Correlation of Carotid Artery Disease Severity and Vasomotor Response of Cerebral Blood Vessels. in Angiology. 2015;66(5):481-487.
doi:10.1177/0003319714538312 .

Krdzic, Ivana, Covickovic-Sternic, Nadezda, Katsiki, Niki, Isenović, Esma R., Radak, Đorđe J., "Correlation of Carotid Artery Disease Severity and Vasomotor Response of Cerebral Blood Vessels" in Angiology, 66, no. 5 (2015):481-487,
https://doi.org/10.1177/0003319714538312 . .

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 . .