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Thrombin‐induced CCN2 expression as a target for anti‐fibrotic therapy in scleroderma
Author(s) -
Leask Andrew
Publication year - 2010
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-009-0082-2
Subject(s) - ctgf , scleroderma (fungus) , medicine , connective tissue , fibrosis , thrombin , pathology , connective tissue disease , growth factor , immunology , disease , autoimmune disease , receptor , platelet , inoculation
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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