Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology
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Аутори
Kypreos, Kyriakos E.Zafirović, Sonja
Petropoulou, Peristera-Ioanna
Bjelogrlic, Predrag
Resanović, Ivana
Traish, Abdul
Isenović, Esma R.
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Estrogens have been recognized, in the last 3 decades, as important hormones in direct and indirect modulation of vascular health. In addition to their direct benefit on cardiovascular health, the presence of esterified estrogen in the lipid core of high-density lipoprotein (HDL) particles indirectly contributes to atheroprotection by significantly improving HDL quality and functionality. Estrogens modulate their physiological activity via genomic and nongenomic mechanisms. Genomic mechanisms are thought to be mediated directly by interaction of the hormone receptor complex with the hormone response elements that regulate gene expression. Nongenomic mechanisms are thought to occur via interaction of the estrogen with membrane-bound receptors, which rapidly activate intracellular signaling without binding of the hormone receptor complex to its hormone response elements. Estradiol in particular mediates early and late endothelial nitric oxide synthase (eNOS) activation via interaction wi...th estrogen receptors through both nongenomic and genomic mechanisms. In the vascular system, the primary endogenous source of nitric oxide (NO) generation is eNOS. Nitric oxide primarily influences blood vessel relaxation, the heart rate, and myocyte contractility. The abnormalities in expression and/or functions of eNOS lead to the development of cardiovascular diseases, both in animals and in humans. Although considerable research efforts have been dedicated to understanding the mechanisms of action of estradiol in regulating cardiac eNOS, more research is needed to fully understand the details of such mechanisms. This review focuses on recent findings from animal and human studies on the regulation of eNOS and HDL quality by estradiol in cardiovascular pathology.
Кључне речи:
endothelial nitric oxide synthase / estrogen receptor / estradiol / high-density lipoprotein / cardiovascular diseasesИзвор:
Journal of Cardiovascular Pharmacology and Therapeutics, 2014, 19, 3, 256-268Финансирање / пројекти:
- Хормонска регулација експресије и активности азот оксид синтазе и натријум-калијумове пумпе у експерименталним моделима инсулинске резистенције, дијабетеса и кардиоваскуларних поремећаја (RS-MESTD-Basic Research (BR or ON)-173033)
DOI: 10.1177/1074248413513499
ISSN: 1074-2484; 1940-4034
PubMed: 24414281
WoS: 000334332800003
Scopus: 2-s2.0-84898962124
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Институција/група
VinčaTY - JOUR AU - Kypreos, Kyriakos E. AU - Zafirović, Sonja AU - Petropoulou, Peristera-Ioanna AU - Bjelogrlic, Predrag AU - Resanović, Ivana AU - Traish, Abdul AU - Isenović, Esma R. PY - 2014 UR - https://vinar.vin.bg.ac.rs/handle/123456789/5954 AB - Estrogens have been recognized, in the last 3 decades, as important hormones in direct and indirect modulation of vascular health. In addition to their direct benefit on cardiovascular health, the presence of esterified estrogen in the lipid core of high-density lipoprotein (HDL) particles indirectly contributes to atheroprotection by significantly improving HDL quality and functionality. Estrogens modulate their physiological activity via genomic and nongenomic mechanisms. Genomic mechanisms are thought to be mediated directly by interaction of the hormone receptor complex with the hormone response elements that regulate gene expression. Nongenomic mechanisms are thought to occur via interaction of the estrogen with membrane-bound receptors, which rapidly activate intracellular signaling without binding of the hormone receptor complex to its hormone response elements. Estradiol in particular mediates early and late endothelial nitric oxide synthase (eNOS) activation via interaction with estrogen receptors through both nongenomic and genomic mechanisms. In the vascular system, the primary endogenous source of nitric oxide (NO) generation is eNOS. Nitric oxide primarily influences blood vessel relaxation, the heart rate, and myocyte contractility. The abnormalities in expression and/or functions of eNOS lead to the development of cardiovascular diseases, both in animals and in humans. Although considerable research efforts have been dedicated to understanding the mechanisms of action of estradiol in regulating cardiac eNOS, more research is needed to fully understand the details of such mechanisms. This review focuses on recent findings from animal and human studies on the regulation of eNOS and HDL quality by estradiol in cardiovascular pathology. T2 - Journal of Cardiovascular Pharmacology and Therapeutics T1 - Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology VL - 19 IS - 3 SP - 256 EP - 268 DO - 10.1177/1074248413513499 ER -
@article{ author = "Kypreos, Kyriakos E. and Zafirović, Sonja and Petropoulou, Peristera-Ioanna and Bjelogrlic, Predrag and Resanović, Ivana and Traish, Abdul and Isenović, Esma R.", year = "2014", abstract = "Estrogens have been recognized, in the last 3 decades, as important hormones in direct and indirect modulation of vascular health. In addition to their direct benefit on cardiovascular health, the presence of esterified estrogen in the lipid core of high-density lipoprotein (HDL) particles indirectly contributes to atheroprotection by significantly improving HDL quality and functionality. Estrogens modulate their physiological activity via genomic and nongenomic mechanisms. Genomic mechanisms are thought to be mediated directly by interaction of the hormone receptor complex with the hormone response elements that regulate gene expression. Nongenomic mechanisms are thought to occur via interaction of the estrogen with membrane-bound receptors, which rapidly activate intracellular signaling without binding of the hormone receptor complex to its hormone response elements. Estradiol in particular mediates early and late endothelial nitric oxide synthase (eNOS) activation via interaction with estrogen receptors through both nongenomic and genomic mechanisms. In the vascular system, the primary endogenous source of nitric oxide (NO) generation is eNOS. Nitric oxide primarily influences blood vessel relaxation, the heart rate, and myocyte contractility. The abnormalities in expression and/or functions of eNOS lead to the development of cardiovascular diseases, both in animals and in humans. Although considerable research efforts have been dedicated to understanding the mechanisms of action of estradiol in regulating cardiac eNOS, more research is needed to fully understand the details of such mechanisms. This review focuses on recent findings from animal and human studies on the regulation of eNOS and HDL quality by estradiol in cardiovascular pathology.", journal = "Journal of Cardiovascular Pharmacology and Therapeutics", title = "Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology", volume = "19", number = "3", pages = "256-268", doi = "10.1177/1074248413513499" }
Kypreos, K. E., Zafirović, S., Petropoulou, P., Bjelogrlic, P., Resanović, I., Traish, A.,& Isenović, E. R.. (2014). Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology. in Journal of Cardiovascular Pharmacology and Therapeutics, 19(3), 256-268. https://doi.org/10.1177/1074248413513499
Kypreos KE, Zafirović S, Petropoulou P, Bjelogrlic P, Resanović I, Traish A, Isenović ER. Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology. in Journal of Cardiovascular Pharmacology and Therapeutics. 2014;19(3):256-268. doi:10.1177/1074248413513499 .
Kypreos, Kyriakos E., Zafirović, Sonja, Petropoulou, Peristera-Ioanna, Bjelogrlic, Predrag, Resanović, Ivana, Traish, Abdul, Isenović, Esma R., "Regulation of Endothelial Nitric Oxide Synthase and High-Density Lipoprotein Quality by Estradiol in Cardiovascular Pathology" in Journal of Cardiovascular Pharmacology and Therapeutics, 19, no. 3 (2014):256-268, https://doi.org/10.1177/1074248413513499 . .