Decreased Smad 7 expression contributes to cardiac fibrosis in the infarcted rat heart

Baiqiu Wang, Jianming Hao, Stephen C. Jones, May Sann Yee, Julie C. Roth, Ian M.C. Dixon

Research output: Contribution to journalArticlepeer-review

127 Scopus citations


We examined the role of the transforming growth factor (TGF)-β1 signaling inhibitor Smad 7 in cardiac fibrosis. TGF-β1 (10 ng/ml) was found to increase cytosolic Smad 7 expression in primary adult rat fibroblasts and induce rapid nuclear export of exogenous Smad 7 in COS-7 cells. Furthermore, overexpression of Smad 7 in primary adult fibroblasts was associated with suppressed collagen type I and III expression. We detected Smad 7, phosphorylated Smad 2, TGF-β type I receptor (TβRI), and TGF-β1 proteins in postmyocardial infarct (MI) rat hearts. In 2 and 4 wk post-MI hearts, Smad 7 and TβRI expression were decreased in scar tissue, whereas TGF-β1 expression was increased in scar and viable tissue. In the 8 wk post-MI heart, Smad 7 expression was decreased in both scar tissue and myocardium remote to the infarct scar. Finally, we confirmed that these changes are paralleled by decreased expression of cytosolic phosphorylated receptor-regulated Smad 2 in 4-wk viable myocardium and in 2- and 4-wk infarct scar tissues. Taken together, our data imply that decreased inhibitory Smad 7 signal in cardiac fibroblasts may play a role in the pathogenesis of cardiac fibrosis in the post-MI heart.

Original languageEnglish (US)
Pages (from-to)H1685-H1696
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5 51-5
StatePublished - 2002


  • Experimental heart failure
  • Myocardial infarction
  • Primary cardiac fibroblasts
  • Transforming growth factor-β

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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