The role of adipokines in systemic sclerosis: a missing link?

Systemic sclerosis is a multiorgan autoimmune disease characterized by vasculopathy and tissue fibrosis of unknown etiology. Recently, adipokines (cell signaling proteins secreted by adipose tissue) have attracted much attention as a cytokine family contributing to the various pathological processes of systemic sclerosis. Adipokines, such as leptin, adiponectin, resistin, adipsin, visfatin or chemerin are a heterogenic group of molecules. Adiponectin exhibits anti-fibrotic features and affects inflammatory reactions. Leptin promotes fibrosis and inflammation. Resistin was linked to vascular involvement in systemic sclerosis. Visfatin was associated with regression of skin lesions in late-stage systemic sclerosis. Chemerin appears as a marker of increased risk of impaired renal function and development of skin sclerosis in the early stage of systemic sclerosis. Vaspin was indicated to have a protective role in digital ulcers development. Novel adipokines—adipsin, apelin, omentin and CTRP-3—are emerging as molecules potentially involved in SSc pathogenesis. Serum adipokine levels may be used as predictive and diagnostic factors in systemic sclerosis. However, further investigations are required to establish firm correlations between distinct adipokines and systemic sclerosis.