JUN promotes hypertrophic skin scarring via CD36 in preclinical in vitro and in vivo models
Michelle Griffin(Stanford University), Mimi R. Borrelli(Stanford University), Julia T. Garcia(Stanford Medicine), Michael Januszyk(Stanford University), Megan E. King(Cal Poly Humboldt), Tristan Lerbs(Stanford Medicine), Lu Cui(Stanford Medicine), Alessandra L. Moore(Stanford University), Abra H. Shen(Stanford University), Shamik Mascharak(Stanford Medicine), Nestor M. Diaz Deleon(Stanford University), Sandeep Adem(Stanford University), Walter L. Taylor(Stanford University), Heather E. desJardins-Park(California Institute for Regenerative Medicine), Marc Gastou(Stanford Medicine), Ronak A. Patel(Stanford University), Bryan Duoto(Stanford University), Jan Sokol(Stanford University), Yuning Wei(Stanford University), Deshka S. Foster(Stanford Medicine), Kellen Chen(Stanford University), Derrick C. Wan(Stanford University), Geoffrey C. Gurtner(Stanford University), H. Peter Lorenz(Stanford University), Howard Y. Chang(Howard Hughes Medical Institute), Gerlinde Wernig(Stanford Medicine), Michael T. Longaker(California Institute for Regenerative Medicine)
Cited by 99Open Access
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.
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