JUN promotes hypertrophic skin scarring via CD36 in preclinical in vitro and in vivo models

This is the authors' abstract. We don't add key points for this paper.

. Blocking CD36 with salvianolic acid B or CD36 knockout model counteracted JUN-mediated fibrosis efficacy in both human fibroblasts and mouse wounds. In summary, JUN is a critical regulator of pathological skin scarring, and targeting its downstream effector CD36 may represent a therapeutic strategy against scarring.