Advances in AngⅡ-induced myocardial fi brosis and its signal transduction mechanism

Cardiac remodeling includes cardiac hypertrophy and myocardial fi brosis (MF). MF is mainly manifested as excessive proliferation of local fi broblasts, deposition of extracellular matrix and disproportionate increase of collagensⅠandⅢ, under the actions of different pathological and physiological factors. The renin-angiotensin-aldosterone system (RAAS) is one of the most important neuroendocrine mechanisms underlying MF. AngⅡ, derived not only from the classical RAAS, but also from the local cardiac myocytes and fi broblasts, is the most important effect factor of RAAS, who exerts biological effects in a paracrine or autocrine manner. AngⅡalso induces complex signal pathway of MF mainly by binding to its specific AT1R, and activates a series of signal molecular pathways of the extracellular signals into the cells, thus producing fi brosis effect.