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. Author manuscript; available in PMC: 2012 Oct 1.
Published in final edited form as: J Mol Cell Cardiol. 2010 Nov 6;51(4):600–606. doi: 10.1016/j.yjmcc.2010.10.033

Figure 3.

Figure 3

The role of TGF-β in hypertrophy, fibrosis and post-infarction cardiac remodeling. A: TGF-β transduces hypertrophic signals in cardiomyocytes and induces myofibroblast transdifferentiation, while promoting matrix deposition and preservation. Although TGF-β inhibition in the pressure-overloaded ventricle may attenuate hypertrophy and reduce fibrosis protecting from diastolic dysfunction, complete loss of TGF-β signaling may result in unopposed matrix degradation, cardiac dilation and systolic dysfunction. B: In the infarcted heart TGF-β may serve as the “master switch” that regulates transition from the inflammatory phase to scar formation. TGF-β suppresses inflammatory mediator synthesis by macrophages while enhancing myofibroblast transdifferentiation and matrix deposition. Thus, timing is a crucial determinant of outcome in pharmacologic interventions targeting the TGF-β system following myocardial infarction.