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Published on: March 24, 2017
Thrombin-induced CCN2 expression as a target for anti-fibrotic therapy in scleroderma
1CIHR Group in Skeletal Development and Remodeling, Division of Oral Biology, Department of Dentistry, Schulich School of Medicine and Dentistry, Dental Sciences Building, University of Western Ontario, London, ON Canada N6A 5C1.
Abstract:
Scleroderma (systemic sclerosis, SSc) is a fibrotic disease for which there is no therapy. CCN2 (connective tissue growth factor, CTGF) is a marker and mediator of fibrosis. Previously, it has been shown that thrombin induces CCN2 expression in fibroblasts. In a recent fascinating report, Bogatkevich et al. (Arthritis Rheum 60:3455-3464, 2009) show that dabigatran, an inhibitor of thrombin action, blocks the overexpression of CCN2 by scleroderma fibroblasts and reverses the contractile phenotype of these cells. These results strongly suggest that dabigatran may be a potential antifibrotic drug for the treatment of fibrosing diseases such as scleroderma.
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