Open AccessPossible strategies for anti‐fibrotic drug intervention in scleroderma
Author(s) -
Leask Andrew
Publication year - 2011
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/s12079-011-0122-6
Subject(s) - medicine , scleroderma (fungus) , drug , intervention (counseling) , intensive care medicine , dermatology , bioinformatics , pathology , pharmacology , biology , inoculation , psychiatry
There are no approved drugs for treating the fibrosis in scleroderma (systemic sclerosis, SSc). Myfibroblasts within connective tissue express the highly contractile protein α–smooth muscle actin (α–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 β (TGFβ), 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)γ also appears to act by intervening in TGFβ signaling. This review discusses these potential candidates for antifibrotic therapy in SSc.