Autophagy and skin wound healing

Abstract

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.

Treatment of Acute Wounds With Recombinant Human-Like Collagen and Recombinant Human-Like Fibronectin in C57BL/6 Mice Individually or in Combination

“…Acute skin injury refers to tissue damage and continuous destruction caused by external action in a short period of time. In the process of wound healing, if it stagnates or worsens or even does not heal for a long time, it may develop into a chronic refractory wound ( Ren et al, 2022 ). Therefore, the effective treatment of early wounds is very important to ensure the stable and orderly repair, and achieve early primary healing.…”

Bioinformatics analysis combined with experiments to verify potential autophagy genes in wound healing

“…Autophagy is present throughout the trauma healing process and plays a role in the inflammatory phase, revascularization phase, re-epithelialization phase, and scar phase to varying degrees (15). The inflammatory phase is the first stage after trauma, during which a large number of inflammatory cells are activated and inflammatory cytokines are released.…”

A Dual-Acting Nitric Oxide Donor and Phosphodiesterase 5 Inhibitor Activates Autophagy in Primary Skin Fibroblasts

“…Indeed, the role of autophagy in regulating the different phases of wound healing is increasingly recognized, although deeper understanding of the molecular mechanisms is necessary to promote a fine-tuned regulation in the different cells and wound-healing stages. Only then would a therapeutic intervention in pathological situations such as refractory wounds be conceivable [ 16 ].…”

“…In this work we apply unbiased expression proteomics to define potential molecular pathways activated by TOP-N53 in primary human skin fibroblasts and keratinocytes. We provide evidence that in primary skin fibroblasts, TOP-N53 is capable of activating autophagy, a catabolic cytoprotective lysosomal degradation pathway that is implicated in proper wound healing [ 16 ]. Thus, TOP-N53 supports wound repair in a multilayered fashion, which might be one reason for the robust responses observed in mice.…”