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Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12710/28742
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dc.contributor.authorTihon Beatricie-Marinela-
dc.date.accessioned2024-10-28T12:50:28Z-
dc.date.accessioned2024-11-18T21:30:36Z-
dc.date.available2024-10-28T12:50:28Z-
dc.date.available2024-11-18T21:30:36Z-
dc.date.issued2024-
dc.identifier.citationTihon Beatricie-Marinela. The role of estrogens in cardiovascular disease. In: Abstract Book. MedEspera 2024. The 10th International Medical Congress for Students and Young Doctors. 24-27 April 2024, Chișinău, Republic of Moldova, p. 334. ISBN 978-9975-3544-2-4.en_US
dc.identifier.isbn978-9975-3544-2-4-
dc.identifier.urihttps://ibn.idsi.md/collection_view/3104-
dc.identifier.urihttp://repository.usmf.md/handle/20.500.12710/28742-
dc.descriptionUniversitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu”, Chişinău, Republica Moldovaen_US
dc.description.abstractIntroduction. Epidemiological studies have shown that 17beta-estradiol (E2) levels are inversely associated with cardiovascular disease (CVD) events in post-menopausal women. This indicates that estrogens have a possible implication in CVD pathogenesis, through their genomic and nongenomic mechanisms of action. Aim of study. Highlighting the role of estrogens and estrogen receptors in cardiovascular disease pathophysiology. Methods and materials. Publications from the last 5 years, from specialized journals of the PubMed databases, were selected and analyzed using the following keywords: estrogen, estrogen receptors, genomic and non-genomic mechanisms, cardiovascular disease. Results. Estrogens, through their specific receptors (ERα, ERβ and GPR30s), displayed prominent effects on cardiovascular disease pathogenesis. Evidence suggests their role in the management of systemic and pulmonary arterial hypertension, protecting against atherogenesis, ischemiareperfusion injury, and safeguarding against heart failure with either reduced or preserved ejection fraction (EF). The specific mechanisms of ERα include reducing sympathetic outflow and endothelial dysfunction, decreasing fibrosis and pulmonary vascular remodeling, preserving EF, and enhancing systolic function. ERβ performs by decreasing vasoconstriction, vascular resistance and hypertrophy, mitigating fibrosis and inflammation, reducing apoptosis and preserving mitochondrial integrity, promoting cardiac angiogenesis and normalizing hemodynamic parameters. GPR30s mechanisms of action encompass relaxation of vascular smooth muscle, influence on nitric oxide synthesis, calcium level regulation, modulating cholesterol levels, and minimizing both inflammation and reactive oxygen species production. Conclusion. Estrogens displayed a possible involvement in managing cardiovascular disease, by reducing both the progression and severity of numerous cardiovascular pathologies through various genomic and non-genomic mechanisms of action. Elucidation of cardio protective mechanisms, determined by estrogens and estrogen receptors, will contribute to the development of effective therapeutic strategies for CVD treatment. associated with cardiovascular disease (CVD) events i n post-menopausal women. This indicates that estrogens have a possible implication in CVD pathogenes is, through their genomic and nongenomic mechanisms of action. Aim of study. Highlighting the role of estrogens and estrogen receptors in cardiovascular disease pathophysiology. Methods and materials. Publications from the last 5 years, from specialized journal s of the PubMed databases, were selected and analyzed using the followi ng keywords: estrogen, estrogen receptors, genomic and non-genomic mechanisms, cardiovascul ar disease. Results. Estrogens, through their specific receptors (ERα, ERβ and GPR30s), displayed prominent effects on cardiovascular disease pathogenesis. Evidence s uggests their role in the management of systemic and pulmonary arterial hypertension, protecting aga inst atherogenesis, ischemiareperfusion injury, and safeguarding against heart failure wi th either reduced or preserved ejection fraction (EF). The specific mechanisms of ER α include reducing sympathetic outflow and endothelial dysfunction, decreasing fibrosis and pulmonary vascular remodeling, preserving EF, and enhancing systolic function. ERβ performs by decreasing vasoconstriction, vascular resist ance and hypertrophy, mitigating fibrosis and inflammation, reducing apoptosis and preserving mitochondrial integrity, promoting cardiac angiogenesis an d normalizing hemodynamic parameters. GPR30s mechanisms of action encompass relaxatio n of vascular smooth muscle, influence on nitric oxide synthesis, calcium level regu lation, modulating cholesterol levels, and minimizing both inflammation and reactive oxygen species product ion. Conclusion. Estrogens displayed a possible involvement in managing ca rdiovascular disease, by reducing both the progression and severity of numerous card iovascular pathologies through various genomic and non-genomic mechanisms of action. El ucidation of cardio protective mechanisms, determined by estrogens and estrogen receptors, wi ll contribute to the development of effective therapeutic strategies for CVD treatment.en_US
dc.publisherInstituţia Publică Universitatea de Stat de Medicină şi Farmacie „Nicolae Testemiţanu” din Republica Moldovaen_US
dc.relation.ispartofMedEspera 2024en_US
dc.titleThe role of estrogens in cardiovascular diseaseen_US
dc.typeOtheren_US
Appears in Collections:MedEspera 2024

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