Abstract
Systemic sclerosis (SSc) or scleroderma is an acquired disorder which typically results in fibrosis of the skin and internal organs [ 1 Korn J.H. Immunologic aspects of scleroderma. Curr Opin Rheumatol. 1989; 1: 479-484 Crossref PubMed Scopus (40) Google Scholar , 2 Mauch C. Krieg T. Fibroblast-matrix interactions and their role in the pathogenesis of fibrosis. Rheum Dis Clin North Am. 1990; 16: 93-107 PubMed Google Scholar , 3 Jelaska A. Arakawa M. Broketa G. Korn J.H. Heterogeneity of collagen synthesis in normal and systemic sclerosis skin fibroblasts: increased proportion of high collagen-producing cells in systemic sclerosis fibroblasts. Arthritis Rheum. 1996; 39: 1338-1346 Crossref PubMed Scopus (103) Google Scholar ]. The pathogenesis of tissue fibrosis may include inflammation, autoimmune attack and vascular damage, resulting in the activation of fibroblasts to produce excessive amounts of various collagens, mainly type I collagen which consists of α1(I) and α2(I) collagen [ [4] LeRoy E.C. Increased collagen synthesis by scleroderma skin fibroblasts in vitro: a possible defect in the regulation or activation of the scleroderma fibroblast. J Clin Invest. 1974; 54: 880-889 Crossref PubMed Scopus (492) Google Scholar ]. However, the mechanism underlying the dysregulation of type I collagen in SSc is still unknown.
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