Through transforming growth factor-β ( TGF-β) effects on cardiomyocytes, mesenchymal and immune cells, plays an important role in the pathogenesis of cardiac remodeling and fibrosis. TGFβoverexpression in the mouse heart is associated with fibrosis and hypertrophy. Endogenous TGF-β plays a critical role in the pathogenesis of cardiac fibrotic and hypertrophic remodeling, and modulates matrix metabolism in the pressure-overloaded heart. In the infarcted heart, TGF-β deactivates inflammatory macrophages, while promoting myofibroblast transdifferentiation and matrix synthesis through Smad3-dependent pathways. Thus,TGF-βmay serve as the master switch for the transition of the infarct from the inflammatory phase to formation of the scar. Because of its crucial role in cardiac remodeling, the TGF-β system may be a promising therapeutic target for patients with heart failure.
Key words:
Transforming growth factor-β; Remodeling; Fibrosis; Smad; Hypertrophy; Angiotensin Ⅱ