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表观遗传修饰在伤口愈合中的作用及潜在治疗方法(综述)

Function of epigenetic modifications in wound healing and potential therapies (Review).

作者信息

Cheng Jing, Qian Weiwei, Chen Fang, Liu Xingqin, Fu Min, Cao Wei, Zhou Yue

机构信息

Emergency Department, Shangjinnanfu Hospital, West China Hospital, Sichuan University, Chengdu, Sichuan 611730, P.R. China.

Party Committee Office, Shangjinnanfu Hospital, West China Hospital, Sichuan University, Chengdu, Sichuan 611730, P.R. China.

出版信息

Int J Mol Med. 2025 Nov;56(5). doi: 10.3892/ijmm.2025.5631. Epub 2025 Sep 12.

DOI:10.3892/ijmm.2025.5631
PMID:40937564
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12457877/
Abstract

Wound healing is a highly coordinated physiological process, which is essential for restoring the structural and functional integrity of damaged tissues. The present review explores the multifaceted roles of epigenetic modifications in wound healing and their potential as therapeutic targets. Epigenetic mechanisms, including DNA methylation, histone modifications, regulation by non‑coding RNAs (ncRNAs) and RNA methylation, influence the speed and quality of wound repair by regulating gene expression, cell function and intercellular signaling. During the hemostasis phase, DNA methylation of genes such as platelet endothelial aggregation receptor 1 can impact platelet function, while histone methylation and acetylation serve critical roles in modulating inflammation and fibroblast activation. ncRNAs, such as microRNAs and long ncRNAs, regulate cell proliferation, collagen deposition and scar formation. N6‑methyladenosine modifications, a type of RNA methylation, impact autophagy and fibrosis through their interaction with YTH domain family proteins. Key epigenetic regulators influence wound healing outcomes, providing valuable insights for the development of novel therapeutic strategies. However, challenges remain in translating these findings into clinical applications due to the complexity of epigenetic networks and the need for precise regulatory tools. Future research should focus on elucidating the cell‑specific and spatiotemporal regulatory mechanisms of epigenetic modifications in wound healing, and exploring their potential as therapeutic targets for reducing scar formation and preventing chronic wounds.

摘要

伤口愈合是一个高度协调的生理过程,对于恢复受损组织的结构和功能完整性至关重要。本综述探讨了表观遗传修饰在伤口愈合中的多方面作用及其作为治疗靶点的潜力。表观遗传机制,包括DNA甲基化、组蛋白修饰、非编码RNA(ncRNA)调控和RNA甲基化,通过调节基因表达、细胞功能和细胞间信号传导来影响伤口修复的速度和质量。在止血阶段,血小板内皮聚集受体1等基因的DNA甲基化会影响血小板功能,而组蛋白甲基化和乙酰化在调节炎症和成纤维细胞活化中起关键作用。ncRNA,如微小RNA和长链ncRNA,调节细胞增殖、胶原蛋白沉积和瘢痕形成。N6-甲基腺苷修饰作为一种RNA甲基化,通过与YTH结构域家族蛋白相互作用影响自噬和纤维化。关键的表观遗传调节因子影响伤口愈合结果,为开发新的治疗策略提供了有价值的见解。然而,由于表观遗传网络的复杂性以及对精确调控工具的需求,将这些发现转化为临床应用仍面临挑战。未来的研究应专注于阐明伤口愈合中表观遗传修饰的细胞特异性和时空调控机制,并探索其作为减少瘢痕形成和预防慢性伤口的治疗靶点的潜力。