Front Biosci (Elite Ed). 2009 Jun 1;1:115-22.

Signaling in fibrosis: targeting the TGF beta, endothelin-1 and CCN2 axis in scleroderma.

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CIHR Group in Skeletal Development and Remodeling, Division of Oral Biology, Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London ON, Canada. Andrew.Leask@schulich.uwo.ca

Abstract

Fibrosis affects organs such as the skin, liver, kidney and lung and is a cause of significant morbidity. There is no therapy for fibrosis. Recent significant molecular insights into the signaling underlying fibrosis have been made. Transforming growth factor beta (TGF beta) signaling is a major contributor to fibrogenesis. The signaling mechanisms through which TGF beta induces fibrogenic responses have been under intense scrutiny. Moreover, the potent pro-fibrotic proteins endothelin-1 (ET-1) and CCN2 (connective tissue growth factor, CTGF) are believed to play an essential role in this process as downstream regulators or co-factors of TGF beta signaling. This review summarizes these recent crucial observations with emphasis on the disease scleroderma.

PMID:: 19482630; [PubMed - indexed for MEDLINE]

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Canadian Institutes of Health Research/Canada

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