JAK-2 as a Novel Mediator of the Profibrotic Effects of Transforming Growth Factor beta in Systemic Sclerosis

Abstract

We demonstrated that JAK-2 is activated in a TGF-dependent manner in SSc. Considering the potent antifibrotic effects of JAK-2 inhibition, our study might have direct translational implications, because inhibitors of JAK-2 are currently being evaluated in clinical trials for myeloproliferative disorders and would also be available for evaluation in patients with SSc.

Keywords

• systemic sclerosis
• fibrosis
• JAK-2
• JAK-2 inhibitors