Autophagy is a lysosome-dependent, self-renewal mechanism that can degrade and recycle cellular components in eukaryotic cells to maintain the stability of the intracellular environment and the cells ability to cope with unfavorable environments. Numerous studies suggest that autophagy participates in regulating various cellular functions and is closely associated with the onset and progression of various diseases. Wound healing is a complex, multistep biological process that involves multiple cell types. Refractory wounds, which include diabetic skin ulcers, can seriously endanger human health. Previous studies have confirmed that autophagy plays an essential role in various phases of wound healing. Specifically, in the inflammatory phase, autophagy has an anti-infection effect and it negatively regulates the inflammatory response, which prevents excessive inflammation from causing tissue damage. In the proliferative phase, local hypoxia in the wound can induce autophagy, which plays a role in anti-apoptosis and anti-oxidative stress and promotes cell survival. Autophagy of vascular endothelial cells promotes wound angiogenesis and that of keratinocytes promotes their differentiation, proliferation and migration, which is conducive to the completion of wound re-epithelialisation. In the remodeling phase, autophagy of fibroblasts affects the formation of hypertrophic scars. Additionally, a refractory diabetic wound may be associated with increased levels of autophagy, and the regulation of mesenchymal stem cell autophagy may improve its application to wound healing. Therefore, understanding the relationship between autophagy and skin wound healing and exploring the molecular mechanism of autophagy regulation may provide novel strategies for the clinical treatment of wound healing.

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自噬与皮肤伤口愈合

自噬是一种依赖溶酶体的自我更新机制，可以降解和回收真核细胞中的细胞成分，以维持细胞内环境的稳定性和细胞应对不利环境的能力。大量研究表明，自噬参与调节多种细胞功能，并与多种疾病的发生和发展密切相关。伤口愈合是一个复杂的多步骤生物过程，涉及多种细胞类型。难治性伤口，包括糖尿病性皮肤溃疡，会严重危害人类健康。以前的研究已经证实，自噬在伤口愈合的各个阶段都起着至关重要的作用。具体来说，在炎症阶段，自噬具有抗感染作用，对炎症反应产生负调节作用，这可以防止过度炎症引起组织损伤。在增殖期，创面局部缺氧可诱导自噬，发挥抗凋亡和抗氧化应激作用，促进细胞存活。血管内皮细胞自噬促进创面血管生成，角质形成细胞自噬促进其分化、增殖和迁移，有利于创面再上皮化的完成。在重塑阶段，成纤维细胞的自噬影响肥厚性瘢痕的形成。此外，难治性糖尿病伤口可能与自噬水平升高有关，间充质干细胞自噬的调节可能会改善其在伤口愈合中的应用。所以，