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Metabolic reprogramming in skin wound healing
Burns & Trauma ( IF 5.3 ) Pub Date : 2024-01-03 , DOI: 10.1093/burnst/tkad047
Zitong Wang 1 , Feng Zhao 2, 3 , Chengcheng Xu 1 , Qiqi Zhang 1 , Haiyue Ren 1 , Xing Huang 4 , Cai He 1 , Jiajie Ma 1 , Zhe Wang 1
Affiliation  

Metabolic reprogramming refers to the ability of a cell to alter its metabolism in response to different stimuli and forms of pressure. It helps cells resist external stress and provides them with new functions. Skin wound healing involves the metabolic reprogramming of nutrients, such as glucose, lipids, and amino acids, which play vital roles in the proliferation, differentiation, and migration of multiple cell types. During the glucose metabolic process in wounds, glucose transporters and key enzymes cause elevated metabolite levels. Glucose-mediated oxidative stress drives the proinflammatory response and promotes wound healing. Reprogramming lipid metabolism increases the number of fibroblasts and decreases the number of macrophages. It enhances local neovascularization and improves fibrin stability to promote extracellular matrix remodelling, accelerates wound healing, and reduces scar formation. Reprogramming amino acid metabolism affects wound re-epithelialization, collagen deposition, and angiogenesis. However, comprehensive reviews on the role of metabolic reprogramming in skin wound healing are lacking. Therefore, we have systematically reviewed the metabolic reprogramming of glucose, lipids, and amino acids during skin wound healing. Notably, we identified their targets with potential therapeutic value and elucidated their mechanisms of action.

中文翻译:

皮肤伤口愈合中的代谢重编程

代谢重编程是指细胞响应不同刺激和压力形式而改变其代谢的能力。它帮助细胞抵抗外部压力并为它们提供新的功能。皮肤伤口愈合涉及营养物质(例如葡萄糖、脂质和氨基酸)的代谢重编程,这些营养物质在多种细胞类型的增殖、分化和迁移中发挥着至关重要的作用。在伤口的葡萄糖代谢过程中,葡萄糖转运蛋白和关键酶导致代谢水平升高。葡萄糖介导的氧化应激驱动促炎反应并促进伤口愈合。重新编程脂质代谢会增加成纤维细胞的数量并减少巨噬细胞的数量。它增强局部新生血管形成,改善纤维蛋白稳定性,促进细胞外基质重塑,加速伤口愈合,减少疤痕形成。重编程氨基酸代谢影响伤口上皮再形成、胶原蛋白沉积和血管生成。然而,缺乏对代谢重编程在皮肤伤口愈合中的作用的全面综述。因此,我们系统地回顾了皮肤伤口愈合过程中葡萄糖、脂质和氨基酸的代谢重编程。值得注意的是,我们确定了具有潜在治疗价值的靶标,并阐明了其作用机制。
更新日期:2024-01-03
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