Abstract 186: CD36 Antagonism Minimizes Skin Scarring By Inhibiting JUN-dependent Fibrotic Pathways Within Fibrogenic Fibroblast Subpopulations

摘要

Purpose: Skin fibrosis is the end result of injury in human skin. In the US alone >100 million new scars are formed every year, and with no therapy able to prevent or reverse skin fibrosis the medico-economic burden is enormous. Excessive fibrosis, as seen in hypertrophic scarring (HTS), can lead to devastating disfigurement and permanent functional loss. Incomplete understanding of the key pathogenic mechanisms driving pathological skin fibrosis has significantly hindered development of effective treatment strategies. We recently identified JUN, the AP-1 transcription factor, as a key driver of global tissue fibrosis. Here we investigate the role of JUN in skin scarring.