Research on the Role of Autophagy in Vascular Endothelial Cells in the Healing of Chronic Refractory Wounds.

IF 4.5 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
Biologics : Targets & Therapy Pub Date : 2026-01-13 eCollection Date: 2026-01-01 DOI:10.2147/BTT.S573844
Lao Riling, Fan Kunyue, Gan Liyan, Wang Yaya, Ni Baoling, Li Jiehui
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引用次数: 0

Abstract

Chronic refractory wounds exhibit a complex etiology characterized by prolonged healing and pathological chronic inflammation, which pose significant challenges to wound recovery and may increase the risk of cancer over time. In recent years, the autophagy mechanism has emerged as a focal point of research. This process is regulated by nutritional status, growth factors, and cellular stress. Autophagy facilitates the removal of damaged organelles and misfolded proteins, recycles nutrients, contributes to immune defense, and aids in the elimination of pathogens. Endothelial autophagy is particularly crucial in the healing of chronic refractory wounds. It may be activated under conditions of ischemia, hypoxia, inflammation, and infection, thereby inhibiting cell proliferation and tissue repair while assisting cells in maintaining homeostasis and managing various stressors. Consequently, investigating the autophagic mechanisms in vascular endothelial cells during chronic refractory wound healing is essential for the development of novel wound treatment strategies.

血管内皮细胞自噬在慢性难治性伤口愈合中的作用研究。
慢性难治性伤口具有复杂的病因,其特点是愈合时间延长和病理性慢性炎症,这对伤口恢复构成了重大挑战,并可能随着时间的推移增加癌症的风险。近年来,自噬机制已成为研究的热点。这一过程受营养状况、生长因子和细胞应激的调节。自噬有助于清除受损的细胞器和错误折叠的蛋白质,循环营养物质,有助于免疫防御,并有助于消除病原体。内皮细胞自噬在慢性难治性伤口的愈合中尤为重要。它可能在缺血、缺氧、炎症和感染的条件下被激活,从而抑制细胞增殖和组织修复,同时帮助细胞维持体内平衡和管理各种应激源。因此,研究慢性难治性伤口愈合过程中血管内皮细胞的自噬机制对于开发新的伤口治疗策略至关重要。
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来源期刊
Biologics : Targets & Therapy
Biologics : Targets & Therapy MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
8.30
自引率
0.00%
发文量
22
审稿时长
16 weeks
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