Key result
TGFβ signaling exerts cardioprotective effects early in myocardial infarction but promotes detrimental apoptosis, hypertrophy, and fibrosis during late post-infarct remodeling.
Targeting specific TGFβ signaling pathways like SMAD or TAK, rather than broad inhibition, may offer therapeutic potential for preventing adverse remodeling after myocardial infarction.
Myocardial infarction is a prevailing cause of death in industrial countries. In spite of the good opportunities we have nowadays in interventional cardiology to reopen the clotted coronary arteries for reperfusion of ischemic areas, post-infarct remodeling emerges and contributes to unfavorable structural conversion processes in the myocardium, finally resulting in heart failure. The growth factor TGFbeta is upregulated during these processes. In this review, an overview on the functional role of TGFbeta-signaling in the process of cardiac remodeling is given, as it can influence apoptosis, fibrosis and hypertrophy thereby predominantly aggravating ischemia/reperfusion injury.
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A 2015 study conducted a review in Myocardial infarction. TGFβ signaling was evaluated. TGFβ signaling exerts cardioprotective effects early in myocardial infarction but promotes detrimental apoptosis, hypertrophy, and fibrosis during late post-infarct remodeling.
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