Abstract
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 TGFβ is upregulated during these processes. In this review, an overview on the functional role of TGFβ signaling in the process of cardiac remodeling is given, as it can influence apoptosis, fibrosis and hypertrophy thereby predominantly aggravating ischemia/reperfusion injury.
Highlights
Gerhild Euler*Reviewed by: Sang-Bing Ong, Universiti Teknologi Malaysia, Malaysia Gaetano Santulli, Columbia, USA
Myocardial infarction is one of the most life-threatening diseases in industrial countries
Post-infarct remodeling is a multifaceted structural conversion process in the myocardium comprising loss of cardiomyocytes by programmed cell death that is accompanied by compensatory induction of hypertrophic growth and fibrosis
Summary
Reviewed by: Sang-Bing Ong, Universiti Teknologi Malaysia, Malaysia Gaetano Santulli, Columbia, USA. 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, resulting in heart failure. The growth factor TGFβ is upregulated during these processes. An overview on the functional role of TGFβ 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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