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

Research output: Contribution to journalArticle

568 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)184-195
Number of pages12
JournalCardiovascular Research
Volume74
Issue number2
DOIs
StatePublished - May 1 2007
Externally publishedYes

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Transforming Growth Factors
Myocardial Infarction
Ventricular Remodeling
Protease Inhibitors
Fibronectins
Cardiac Myocytes
Extracellular Matrix
Myocardium
Fibrosis
Collagen
Fibroblasts
Phenotype
Gene Expression
Growth
Genes

Keywords

  • Cytokines
  • Fibrosis
  • Growth factors
  • Infarction
  • Remodeling

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

The role of TGF-β signaling in myocardial infarction and cardiac remodeling. / Bujak, Marcin; Frangogiannis, Nikolaos G.

In: Cardiovascular Research, Vol. 74, No. 2, 01.05.2007, p. 184-195.

Research output: Contribution to journalArticle

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