Научные статьиM.H.Sayidova, S.U.Pulatova2025
HYPERTENSION-INDUCED CARDIOVASCULAR REMODELING: MECHANISMS, CLINICAL IMPLICATIONS, AND MODERN THERAPEUTIC INTERVENTIONS
Umarov Sherali Berdibayevich · Aminov Azimjon Alijon o‘g‘li · Axmedov Abbos Botir o‘g‘li · Functional Diagnostics! Second-year clinical residents. (¹'²'³Samarkand State Medical University DKTF, Department of Internal Medicine, Cardiology and)
Современная наука и исследования · 2025
Аннотация
Hypertension is widely recognized as a principal modifiable risk factor for cardiovascular disease (CVD) and a major contributor to premature morbidity and mortality worldwide. The persistent elevation of arterial pressure exerts hemodynamic stress on the heart and vasculature, leading to a cascade of structural and functional alterations collectively known as cardiovascular remodeling. The aim of this research is to provide an in-depth analysis of the molecular and physiological mechanisms underlying hypertension-induced remodeling and to evaluate contemporary therapeutic strategies aimed at reversing or attenuating this pathological process. Cardiovascular remodeling encompasses changes in the heart (e.g., left ventricular hypertrophy, interstitial fibrosis, and diastolic dysfunction), as well as vascular changes (e.g., arterial wall thickening, increased stiffness, endothelial dysfunction, and microvascular rarefaction). These alterations, initially adaptive, become maladaptive over time, increasing the risk of heart failure, arrhythmias, myocardial infarction, stroke, and sudden cardiac death.
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«Hypertension is widely recognized as a principal modifiable risk factor for cardiovascular disease (CVD) and a major contributor to premature morbidity and mortality worldwide.»
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Демо-превьюHypertension is widely recognized as a principal modifiable risk factor for cardiovascular disease (CVD) and a major contributor to premature morbidity and mortality worldwide. Полный текст публикации CiteX не хранит — доступ к первоисточнику открывается по DOI согласно лицензии издателя и выбранному плану.
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- calcineurin-NFAT, The pathogenesis of remodeling begins with pressure overload triggering myocardial hypertrophy through mechanical stretch and neurohormonal activation. Angiotensin II, norepinephrine, and endothelin-1 act as key mediators, aldosterone, and Akt-mTOR that promote protein synthesis and cardiomyocyte hypertrophy, activating intracellular signaling pathways such as mitogen-activated protein kinases (MAPKs)
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