Published in

American Association for the Advancement of Science, Science Translational Medicine, 609(13), 2021

DOI: 10.1126/scitranslmed.abb3312

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

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

Full text: Unavailable

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Preprint: archiving allowed
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Postprint: archiving allowed
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Data provided by SHERPA/RoMEO

Abstract

JUN drives scarring by modifying the roles of fibroblast subpopulations, and JUN antagonism via CD36 may represent an antiscarring therapy.