Considered in the light of these findings, hypo adiponectin coupled with reduced AdipoR1 expression in scleroderma patients with early diffuse disease suggest that attenuated adiponectin signaling is a risk factor directly contributing to the failure to control aberrant fibrogenic responses, resulting in persistent fibroblast activation and sustained collagen production and myofibroblast differentiation. Here, ADIPOR1 is linked to scleroderma.