Elucidating the dual roles of apoptosis and necroptosis in diabetic wound healing: implications for therapeutic intervention

Xingqian Wu , Rifang Gu , Ming Tang , Xingrui Mu , Wenjie He , Xuqiang Nie

Burns & Trauma ›› 2025, Vol. 13 ›› Issue (1) : tkae061

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Burns & Trauma ›› 2025, Vol. 13 ›› Issue (1) :tkae061 DOI: 10.1093/burnst/tkae061
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Elucidating the dual roles of apoptosis and necroptosis in diabetic wound healing: implications for therapeutic intervention
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Abstract

Wound healing is a complex and multistep biological process that involves the cooperation of various cell types. Programmed cell death, including apoptosis and necrotizing apoptosis, plays a crucial role in this process. Apoptosis, a controlled and orderly programmed cell death regulated by genes, helps eliminate unnecessary or abnormal cells and maintain internal environmental stability. It also regulates various cell functions and contributes to the development of many diseases. In wound healing, programmed cell death is essential for removing inflammatory cells and forming scars. On the other hand, necroptosis, another form of programmed cell death, has not been thoroughly investigated regarding its role in wound healing. This review explores the changes and apoptosis of specific cell groups during wound healing after an injury and delves into the potential underlying mechanisms. Furthermore, it briefly discusses the possible mechanisms linking wound inflammation and fibrosis to apoptosis in wound healing. By understanding the relationship between apoptosis and wound healing and investigating the molecular mechanisms involved in apoptosis regulation, new strategies for the clinical treatment of wound healing may be discovered.

Keywords

Apoptosis / Necroptosis / Wound healing / Inflammation / Therapeutic intervention

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Xingqian Wu, Rifang Gu, Ming Tang, Xingrui Mu, Wenjie He, Xuqiang Nie. Elucidating the dual roles of apoptosis and necroptosis in diabetic wound healing: implications for therapeutic intervention. Burns & Trauma, 2025, 13 (1) : tkae061 DOI:10.1093/burnst/tkae061

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