Significance Chronic wounds (CWs) are a major healthcare challenge, characterized by persistent inflammation that fails to resolve naturally. We found that dysregulation of the proresolving POMC–MC1R pathway is a common feature across different types of CWs including diabetic ulcers and pressure sores. Using a mouse model that replicates human CWs, we demonstrated that targeting MC1R with a topical drug promotes healing by improving blood vessel formation, reducing neutrophil recruitment and NET formation to restore tissue repair. By identifying MC1R as a central regulator of wound repair, we provide a promising therapeutic strategy that could benefit millions of patients suffering from nonhealing wounds.
MC1R determines healing outcomes in acute and chronic cutaneous wounds
Yonlada Nawilaijaroen,Holly R. Rocliffe,Shani Austin-Williams,Georgios Krilis,Charlotte H Dawson,Pruistinne Harijanto,Antonella Pellicoro,Kanheng Zhou,Yubo Ji,Connor Bain,Alastair M. Kilpatrick,Yuhang Chen,Asok Biswas,Shareen Forbes,Michael Crichton,Zhihong Huang,Stuart J. Forbes,Andrea Caporali,Jenna L Cash
Published 2025 in Proceedings of the National Academy of Sciences of the United States of America
ABSTRACT
PUBLICATION RECORD
- Publication year
2025
- Venue
Proceedings of the National Academy of Sciences of the United States of America
- Publication date
2025-11-11
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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