An increased transforming growth factor β receptor type I:Type II ratio contributes to elevated collagen protein synthesis that is resistant to inhibition via a kinase‐deficient transforming growth factor β receptor type II in scleroderma

Abstract

This study indicates that an increased TGFbetaRI:TGFbetaRII ratio may underlie aberrant TGFbeta signaling in SSc and contribute to elevated basal collagen production, which is insensitive to TGFbeta signaling blockade via DeltakRII.