Mechanical stretch of cardiac myocytes activates multiple second messenger systems and stimulates rapid secretion of angiotensin II, mediating hypertrophic responses in vitro.
This review highlights how mechanical stretch in cardiac myocytes activates intracellular signaling and the local renin-angiotensin system to induce hypertrophy.
External load plays a critical role in determining muscle mass and its phenotype in cardiac myocytes. Cardiac myocytes have the ability to sense mechanical stretch and convert it into intracellular growth signals, which lead to hypertrophy. Mechanical stretch of cardiac myocytes in vitro causes activation of multiple second messenger systems that are very similar to growth factor-induced cell signaling systems. Stretch of neonatal rat cardiac myocytes stimulates a rapid secretion of angiotensin II which, together with other growth factors, mediates stretch-induced hypertrophic responses in vitro. In this review, various cell signaling mechanisms initiated by mechanical stress on cardiac myocytes are summarized with emphasis on potential mechanosensing mechanisms and the relationship between mechanical loading and the cardiac renin-angiotensin system.
Sadoshima et al. (1997) conducted a review in Cardiac hypertrophy. Mechanical stress was evaluated. Mechanical stretch of cardiac myocytes activates multiple second messenger systems and stimulates rapid secretion of angiotensin II, mediating hypertrophic responses in vitro.