抑制USP7通过通过NF-κB/MAPK信号通路抑制M1巨细胞极化促进伤口愈合

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Shami Aihemaiti¹, Kang Wei², Dilihumaer Abulimiti¹

¹Department of Orthopedic Trauma and Microsurgery, Zhongnan Hospital of Wuhan University, Wuhan 430071, PR China.

International immunopharmacology

|November 8, 2025

概括

在临床前模型中,抑制Ubiquitin特异性酶7 (USP7) 降低了促炎性M1巨分化,促进纤维细胞活性,增强伤口愈合和血管生成.

科学领域:

生物医学研究的研究.
细胞生物学细胞生物学
伤口愈合研究研究研究

背景情况:

慢性伤口带来了重大的临床和经济挑战.
乌比基特异性酶7 (USP7) 与瘤微环境中的巨细胞两极分化有关.
在伤口炎症期间,USP7在巨细胞两极分化中的作用尚不清楚.

研究的目的:

调查乌比基特异性酶7 (USP7) 在调节M1巨分化中的作用.
阐明USP7在伤口愈合中的潜在机制.
评估USP7抑制在伤口管理中的治疗潜力.

主要方法:

在体外和体外模型被用于研究USP7.7.
通过测量促炎性细胞因子水平 (IL-1β,IL-6,TNF-α) 来评估巨细胞极化.
在USP7淘汰赛巨中分析了NF-κB和MAPK信号通路.
评估了纤维细胞迁移和增殖.
用小鼠伤口愈合模型来评估治疗疗效和血管生成.

主要成果:

抑制USP7显著降低了M1巨细胞两极分化和促炎性细胞因子的产生.
在骨髓衍生的巨细胞 (BMDM) 中USP7淘汰抑制了NF-κB和MAPK信号通路.
在炎症环境中,USP7淘汰赛促进了纤维细胞迁移和增殖.
在BMDM中USP7淘汰的小鼠表现出改善的伤口愈合效率和增强的血管生成.

结论:

在伤口炎症中,USP7在促进M1巨细胞两极分化方面发挥着关键作用.
抑制USP7将巨细胞转移到抗炎表型,并支持组织修复.
针对USP7提供了一种有前途的治疗策略,可以改善慢性伤口愈合和组织再生.

关键词:

炎症炎症是一种炎症.这就是MAPKK.巨细胞是一个巨细胞.在 NF-κBB 中.伤口愈合伤口愈合

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