JUN promotes hypertrophic skin scarring via CD36 in preclinical in vitro and in vivo models
Michelle Griffin, Mimi R. Borrelli, Julia T. Garcia, Michael Januszyk, Megan E. King, Tristan Lerbs, Lu Cui, Alessandra L. Moore, Abra H. Shen, Shamik Mascharak, Nestor M. Diaz Deleon, Sandeep Adem, Walter L. Taylor, Heather E. desJardins-Park, Marc Gastou, Ronak A. Patel, Bryan Duoto, Jan Sokol, Yuning Wei, Deshka S. Foster, Kellen Chen, Derrick C. Wan, Geoffrey C. Gurtner, H. Peter Lorenz, Howard Y. Chang, Gerlinde Wernig, Michael T. Longaker
Abstract
. 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.