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Possible strategies for anti-fibrotic drug intervention in scleroderma Leask AJ Cell Commun Signal 2011[Jun]; 5 (2): 125-9There are no approved drugs for treating the fibrosis in scleroderma (systemic sclerosis, SSc). Myfibroblasts within connective tissue express the highly contractile protein alpha-smooth muscle actin (alpha-SMA) and are responsible for the excessive synthesis and remodeling of extracellular matrix (ECM) characterizing SSc. Drugs targeting myofibroblast differentiation, recruitment and activity are currently under consideration as anti-fibrotic treatments in SSc but thus far have principally focused on the transforming growth factor beta (TGFbeta), endothelin-1 (ET-1), connective tissue growth factor (CCN2/CTGF) and platelet derived growth factor (PDGF) pathways, which display substantial signaling crosstalk. Moreover, peroxisome proliferator-activated receptor (PPAR)gamma also appears to act by intervening in TGFbeta signaling. This review discusses these potential candidates for antifibrotic therapy in SSc.ä |
