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• W140993434 startingPage "111" @default.
• W140993434 abstract "SummaryCardiac hypertrophy is a common outcome of hypertension or myocardial infarction and a major contributor to cardiovascular morbidity and mortality. Under conditions of increased hemodynamic load, the heart compensates by undergoes compensatory hypertrophy, a response that restores lost function and normalizes wall stress. It is thus very important to understand the molecular mechanisms responsible for the development of cardiac hypertrophy. In isolated cardiac myocytes, mechanical stretch induces activation of several protein kinases, fetal gene expression, upregulation of renin-angiotensin system components and cellular hypertrophy. Pretreatment with an angiotensin II (Ang II) type II receptor blockers significantly attenuates all of the mechanical stretch induced events. Many animal and clinical studies have shown that blockade of the RAS with AT1 receptor blocker or angiotensin converting enzyme inhibitor induce regression of cardiac hypertrophy and prevent progression of heart failure, resulting in a reduction in cardiac morbidity and mortality. These studies indicate that the local RAS is activated by hemodynamic overload and that the AT1 receptor has a crucial role in the development of load-induced cardiac hypertrophy. Although it is evident that mechanical stress is the primary trigger of cardiac hypertrophy, it is not clear how mechanical stimuli is sensed and converted into intracellular signals. Integrins and associated signaling machinery have been reported to be sensors for mechanical stress. Below, we focus on evidence for integrins as the mechanosensors and mechanotransduction systems responsible for cardiac hypertrophy and activators of the cardiac RAS." @default.
• W140993434 created "2016-06-24" @default.
• W140993434 creator A5020208896 @default.
• W140993434 creator A5069116806 @default.
• W140993434 date "2006-01-25" @default.
• W140993434 modified "2023-09-26" @default.
• W140993434 title "Mechanical Signaling and the Cardiac Renin-angiotensin" @default.
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