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MC1R决定了急性和慢性皮肤伤口的愈合结果

Yonlada Nawilaijaroen¹, Holly R Rocliffe¹, Shani Austin-Williams²

¹Centre for Inflammation Research, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh EH16 4UU, United Kingdom.

Proceedings of the National Academy of Sciences of the United States of America

|November 11, 2025

概括

功能障碍的亲opiomelanocortin-melanocortin 1受体 (POMC-MC1R) 信号影响慢性伤口愈合. 通过激动剂向MC1R,通过减少炎症和增强组织再生,促进修复.

科学领域:

皮肤病学皮肤病学
伤口治愈研究研究伤口治愈研究
分子医学是分子医学.

背景情况:

慢性伤口 (CWs) 呈现持久性炎症和未能修复的情况,前溶解途径功能障碍在很大程度上尚未探索.
亲opiomelanocortin-melanocortin 1受体 (POMC-MC1R) 轴与炎症反应有关,但其在CW中的作用尚不清楚.

研究的目的:

研究POMC-MC1R轴在慢性伤口病理生理学的作用.
评估MC1R激动剂在促进慢性伤口愈合方面的治疗潜力.

主要方法:

利用缺乏功能性MC1R的MC1Re/e小鼠来建模受损伤愈合.
开发了一种模仿人类病理学的新鼠慢性伤口模型.
在伤口模型中局部使用选择性MC1R激动剂 (BMS-470539).
评估伤口愈合参数,包括重新上皮化,排泄物,血管化和中性粒细胞外陷 (NETosis).

主要成果:

小鼠的MC1R缺乏导致了延迟的再上皮化和增加的NETosis,反映了人类CW特征.
在小鼠CW模型中,局部MC1R激动剂治疗通过减少排泄物,增强血管化和促进重新上皮化来恢复愈合.
MC1R激动剂改善了伤床 perfusion 和淋巴排水通过血管生成和淋巴血管生成,同时减少痕.
MC1Re/e小鼠表现出的严重程度加剧,排泄物增加和NETosis增加.

结论:

POMC-MC1R轴是皮肤修复过程的关键调节器.
MC1R的失调有助于慢性伤口的病理学.
MC1R激动剂代表了一种有前途的治疗策略,可以加速慢性伤口愈合.

关键词:

慢性慢性慢性慢性这是一种炎症炎症炎症炎症.解决方案的解决方案解决方案的解决方案.皮肤皮肤皮肤伤口的伤口是伤口.

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