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Cardiovascular Research 2007 74(2):207-212; doi:10.1016/j.cardiores.2006.07.012
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Copyright © 2006, European Society of Cardiology

TGFβ, cardiac fibroblasts, and the fibrotic response

Andrew Leask*

CIHR Group in Skeletal Development and Remodeling, Division of Oral Biology and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, Dental Sciences Building, London ON, Canada N6A 5C1

* Tel.: +1 519 661 2111x81102. Email address: Andrew.Leask{at}schulich.uwo.ca

The cytokine transforming growth factor β (TGFβ) is a major contributor to fibrogenic responses both in vitro and in vivo. TGFβ possesses many functions; thus, broadly targeting TGFβ signaling as an anti-fibrotic approach is anticipated to be problematic. Recent experiments, however, have begun to elucidate the signaling pathways through which TGFβ activates a fibrotic program. This review critically evaluates the evidence supporting TGFβ as a pro-fibrotic cytokine, with special attention to cardiac fibrosis, and suggests several possible points for selective drug intervention to combat chronic fibrotic disease.

KEYWORDS TGFbeta; Fibrosis; Endothelin; CTGF

Time for primary review 32 days


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