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Cardiovascular Research 2007 74(2):184-195; doi:10.1016/j.cardiores.2006.10.002
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Copyright © 2006, European Society of Cardiology

The role of TGF-β signaling in myocardial infarction and cardiac remodeling

Marcin Bujak and Nikolaos G. Frangogiannis*

Section of Cardiovascular Sciences, One Baylor Plaza M/S F-602, Baylor College of Medicine, Houston, TX 77030, USA
Methodist DeBakey Heart Center, Houston, TX, USA

* Corresponding author. Section of Cardiovascular Sciences, One Baylor Plaza M/S F-602, Baylor College of Medicine, Houston, TX 77030, USA. Tel.: +1 713 798 4188; fax: +1 713 796 0015. Email address: ngf{at}bcm.tmc.edu

Transforming Growth Factor (TGF)-β is markedly induced and rapidly activated in the infarcted myocardium. However, understanding of the exact role of TGF-β signaling in the infarcted and remodeling heart has been hampered by the complex and unusual biology of TGF-β activation and by the diversity of its effects eliciting multiple, and often opposing cellular responses. Experimental studies suggest that TGF-β signaling may be crucial for repression of inflammatory gene synthesis in healing infarcts mediating resolution of the inflammatory infiltrate. In addition, TGF-β may play an important role in modulating fibroblast phenotype and gene expression, promoting extracellular matrix deposition in the infarct by upregulating collagen and fibronectin synthesis and by decreasing matrix degradation through induction of protease inhibitors. TGF-β is also a key mediator in the pathogenesis of hypertrophic and dilative ventricular remodeling by stimulating cardiomyocyte growth and by inducing interstitial fibrosis. In this review we summarize the current knowledge on the role of TGF-β in infarct healing and cardiac remodeling.

KEYWORDS Fibrosis; Growth factors; Infarction; Remodeling; Cytokines

Time for primary review 38 days


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