近端肾小管上皮细胞代谢重编程在急性肾损伤中的研究进展  

Metabolic reprogramming of proximal renal tubular epithelial cells in acute kindey injury

作　　者：郑星月 周芳芳(综述)[2] 罗群(审校)[2] ZHENG Xingyue;ZHOU Fangfang;LUO Qun(Health Science Center,Ningbo University,Ningbo 315211,China;Department of Nephrology,Ningbo No.2 Hospital,Ningbo 315010,China)

机构地区：[1]宁波大学医学部,宁波315211 [2]宁波市第二医院肾内科

出　　处：《肾脏病与透析肾移植杂志》2024年第1期59-63,共5页Chinese Journal of Nephrology,Dialysis & Transplantation

基　　金：浙江省宁波市共建医学重点学科资助(2022-S03);浙江省公益技术应用研究(LGF22H050009);浙江省自然科学青年基金(LQ19H050001);浙江省医药卫生科技计划项目(2021KY296)。

摘　　要：肾脏是一个高代谢器官,尤其是近端肾小管上皮细胞,在生理情况下主要依赖脂肪酸氧化供能,但是在急性肾损伤(AKI)期间,线粒体和过氧化物酶体功能障碍,近端肾小管上皮细胞发生代谢重编程,能量供应转向糖酵解,生成乳酸,并伴脂肪酸氧化紊乱及糖异生受损,短期内代谢重编程可能是对肾脏有益的能量代偿,但是该过程中也会加重肾损伤。本文就近端肾小管上皮细胞代谢重编程在AKI中的作用进行综述。The kidney is a highly metabolic organ,especially the proximal renal tubular epithelial cells,which mainly rely on fatty acid oxidation for energy supply under physiological conditions.However,when acute kidney injury(AKI)occurs,mitochondrial and peroxisome dysfunction causes metabolic reprogramming of proximal renal tubular epithelial cells,and the energy supply turns to glycolysis and lactate production,accompanied by fatty acid oxidation disorder and impaired gluconeogenesis.Metabolic reprogramming may be a beneficial energy compensation for kidney in the short term.However,this process also aggravates kidney damage.This article reviews the role of metabolic reprogramming of proximal renal tubular epithelial cells in AKI.

关 键 词：急性肾损伤 代谢重编程 近端肾小管上皮细胞 

分 类 号：R692[医药卫生—泌尿科学]