S100A4 amplifies TGF-{beta}-induced fibroblast activation in systemic sclerosis

Conclusions
We characterised S100A4 as a downstream mediator of the stimulatory effects of TGF-β on fibroblasts in SSc. TGF-β induces the expression of S100A4 to stimulate the release of collagen in SSc fibroblasts and induce fibrosis. Since S100A4 is essentially required for the pro-fibrotic effects of TGF-β and neutralising antibodies against S100A4 are currently evaluated, S100A4 might be a candidate for novel antifibrotic therapies.

Source: Annals of the Rheumatic Diseases - August 10, 2015 Category: Rheumatology Authors: Tomcik, M., Palumbo-Zerr, K., Zerr, P., Avouac, J., Dees, C., Sumova, B., Distler, A., Beyer, C., Cerezo, L. A., Becvar, R., Distler, O., Grigorian, M., Schett, G., Senolt, L., Distler, J. H. W. Tags: Immunology (including allergy), Connective tissue disease Basic and translational research Source Type: research