首页|急性肾损伤SIRT3信号调控及中医药作用研究进展

急性肾损伤SIRT3信号调控及中医药作用研究进展

扫码查看
原文链接
  • 万方数据
  • 维普
急性肾损伤(acute kidney injury,AKI)是世界范围内的一个重大的公共卫生问题,其短期预后差,增加了终末期肾病(end stage renal disease,ESRD)的风险,患病率及死亡率较高.因此,深入探讨AKI的潜在调控机制对于改善其预后至关重要.沉默信息调控因子3(silent information regulator 3,SIRT3)可通过脱乙酰化并介导多种信号通路中的蛋白质底物调节线粒体代谢、氧化应激、炎症反应、细胞凋亡、细胞自噬,从而预防AKI,有望成为潜在的治疗新靶点.多种中药单体、中药复方可通过调控SIRT3相关通路发挥肾脏保护作用,是AKI的研究热点.因此,以SIRT3为着眼点,就中医药通过调控SIRT3相关通路干预AKI的分子机制进行综述,以期为AKI的防治提供新的思路,为中药新药的研发与应用提供依据.
Research progress on regulation of SIRT3 signal and the role of Chinese medicine in acute kidney injury
Acute kidney injury(AKI)is a significant public health issue worldwide,with poor short-term prognosis,increased risk of end stage renal disease(ESRD),and high morbidity and mortality.Therefore,it is crucial to delve deeply into the potential regulatory mechanisms of AKI to improve its prognosis.The silent information regulator 3(SIRT3)can regulate mitochondrial metabolism,oxidative stress,inflammatory response,apoptosis,and autophagy through deacetylation and mediation of protein substrates in various signaling pathways,thus preventing AKI and offering a potential therapeutic target.A variety of Chinese medicine monomers and compound formulas can exert renal protective effects by regulating SIRT3-related pathways,making them a research hotspot in AKI.Therefore,focusing on SIRT3,this review summarizes the molecular mechanisms of Chinese medicine in interventing AKI by regulating SIRT3-related pathways,aiming to provide new ideas for the prevention and treatment of AKI and provide a basis for the research,development,and application of new Chinese medicines.

acute kidney injurysilent information regulator 3Chinese medicinesignaling pathwayresearch progressmolecular mechanism

刘馥溧、巴元明

展开 >

湖北中医药大学,湖北 武汉 430061

湖北中医药大学附属医院/湖北省中医院肾内科,湖北 武汉 430061

急性肾损伤 沉默信息调控因子3 中医药 信号通路 研究进展 分子机制

全国名老中医药专家传承工作室建设项目(巴元明全国名老中医药专家传承工作室)第六批全国老中医药专家学术经验继承工作指导老师项目

国中医药人教函[2022]75号国中医药人教发[2017]29号

2024

10.3969/j.issn.1674-070X.2024.04.030

湖南中医药大学学报
湖南中医药大学

湖南中医药大学学报

CSTPCD
影响因子：1.098
ISSN：1674-070X
年,卷(期)：2024.44(4)
  • 57