期刊
BURNS & TRAUMA
卷 10, 期 -, 页码 -出版社
OXFORD UNIV PRESS
DOI: 10.1093/burnst/tkac003
关键词
Autophagy; Wound healing; Diabetes; Mesenchymal stem cells; microRNA; Skin
资金
- National Natural Science Foundation of China [81601692, 81901969]
- Technology Research from the Department of Education of Liaoning Province [JCZR2020013]
- 345 Talent Project of Shenjing hospital of China Medical University
The article discusses the role of autophagy in wound healing, including its anti-infection and inflammation regulatory functions in the inflammatory phase, its promotion of cell survival, angiogenesis, and cell differentiation in the proliferative phase, and its impact on hypertrophic scar formation in the remodeling phase. The article also highlights the association between autophagy and refractory diabetic wounds, and suggests that understanding autophagy regulation and molecular mechanisms can provide novel strategies for wound healing treatment.
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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