Contribution of Adipocytes and Adipokines to Fibrosis and Severe Disease Manifestations in Systemic Sclerosis

The objective of the K12 application is to link severe SSc organ manifestations to adipose-derived metabolic parameters to better understand disease pathogenesis and identify novel biomarkers. The central hypothesis is that decreased PPAR-γ in adipocytes is a central mechanism in SSc and that this leads to alterations in adipokine signaling (increased leptin and decreased adiponectin) which mediate fibrosis and other organ pathologies. Funds from the Hoellen Foundation will provide support to conduct experiments where additional metabolic studies, biochemical analyses, and immunohistochemical stains would be very helpful to the K12 project.