JUN promotes hypertrophic skin scarring via CD36 in preclinical in vitro and in vivo models-Reference-Cited by-同舟云学术

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

Published:2021-09 Issue:609 Volume:13 Page:
ISSN:1946-6234
Container-title:Science Translational Medicine
language:en
Short-container-title:Sci. Transl. Med.

Author:

Griffin Michelle F.¹^ORCID,Borrelli Mimi R.¹^ORCID,Garcia Julia T.²³,Januszyk Michael¹,King Megan¹⁴,Lerbs Tristan⁵,Cui Lu⁵^ORCID,Moore Alessandra L.¹^ORCID,Shen Abra H.¹^ORCID,Mascharak Shamik¹⁵^ORCID,Diaz Deleon Nestor M.¹,Adem Sandeep¹,Taylor Walter L.¹^ORCID,desJardins-Park Heather E.¹⁶^ORCID,Gastou Marc⁵^ORCID,Patel Ronak A.¹,Duoto Bryan A.¹,Sokol Jan¹^ORCID,Wei Yuning²,Foster Deshka¹⁵^ORCID,Chen Kellen¹^ORCID,Wan Derrick C.¹^ORCID,Gurtner Geoffrey C.¹^ORCID,Lorenz Hermann P.¹^ORCID,Chang Howard Y.²³⁷^ORCID,Wernig Gerlinde⁵⁶^ORCID,Longaker Michael T.¹⁶^ORCID

Affiliation:

1. Hagey Laboratory of Pediatric Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.

2. Center for Personal Dynamics Regulomes, Stanford University School of Medicine, Stanford, CA 94305, USA.

3. Department of Genetics, Stanford School of Medicine, Stanford, CA 94305, USA.

4. CIRM Scholars Program, Humboldt State University, Arcata, CA 95521, USA.

5. Department of Pathology, Stanford School of Medicine, Stanford, CA 94305, USA.

6. Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305, USA.

7. Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.

Abstract

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

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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