TGFβ—a role in systemic sclerosis?

✍ Scribed by Cotton, Shirley A.; Herrick, Ariane L.; Jayson, Malcolm I. V.; Freemont, Anthony J.

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 39 KB
• Volume: 184
• Category: Article
• ISSN: 0022-3417
• DOI: 10.1002/(sici)1096-9896(199801)184:1<4::aid-path968>3.0.co;2-0

✦ Synopsis

Systemic sclerosis (SSc) is a multisystem connective tissue disorder in which there is progressive fibrosis. Transforming growth factor beta (TGF ) has wide-ranging cellular actions. It is a potent chemoattractant for human dermal fibroblasts, from which it may induce synthesis of collagen, which suggests that it may have a central role to play in the pathogenesis of SSc. This is supported to some extent by in vitro studies. SSc fibroblasts produce more collagens and fibronectin than normal fibroblasts and elevated TIMP levels have been observed, all of which could be explained on the basis of TGF stimulation of fibroblasts. Some studies have suggested that fibroblasts are the source of TGF . However, the serum of patients with SSc is cytotoxic to endothelial cells, which could culminate in TGF synthesis by them, with secondary fibroblast stimulation. The role of TGF remains elusive, although it would seem an ideal candidate as a mediator of fibrosis in systemic sclerosis. 1998