TGFbeta, cardiac fibroblasts, and the fibrotic response.
The cytokine transforming growth factor beta (TGFbeta) is a major contributor to fibrogenic responses both in vitro and in vivo. TGFbeta possesses many functions; thus, broadly targeting TGFbeta signaling as an anti-fibrotic approach is anticipated to be problematic. Recent experiments, however, have begun to elucidate the signaling pathways through which TGFbeta activates a fibrotic program. This review critically evaluates the evidence supporting TGFbeta 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.
Leask
Andrew
A
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, London ON, Canada N6A 5C1. andrew.leask@schulich.uwo.ca
D000809:Angiotensins / Q000378:metabolism; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D005355:Fibrosis; D006801:Humans; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018125:Receptors, Transforming Growth Factor beta / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000276:immunology / Q000378:metabolism*
D000809:Angiotensins; D016207:Cytokines; D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta