Dysregulation of transforming growth factor β signaling in scleroderma: Overexpression of endoglin in cutaneous scleroderma fibroblasts

Abstract

SSc is characterized by overproduction of matrix; that is, genes that are targets of TGF beta signaling in normal fibroblasts. Our findings suggest that lesional SSc fibroblasts may overexpress endoglin as a negative feedback mechanism in an attempt to block further induction of profibrotic genes by TGF beta.