These data demonstrate that JunD is overexpressed in SSc and that JunD is a mediator of the profibrotic effects of TGFbeta. Considering that inhibitors of AP-1 signalling have recently been These data demonstrate that JunD is overexpressed in SSc and that JunD is a mediator of the profibrotic effects of TGFbeta.
Considering that inhibitors of AP-1 signalling have recently been developed and are available for clinical trials in SSc, these findings may have translational implications.