Dysfunctional glucose metabolism triggers oxidative stress to induce kidney injury in diabetes  

作　　者：Meng Gao Meng-Ting Dai Guo-Hua Gong 

机构地区：[1]School of Laboratory Medicine and Life Sciences,Wenzhou Medical University,Wenzhou 325035,Zhejiang Province,China [2]Institute for Regenerative Medicine,Shanghai East Hospital,School of Life Sciences and Technology,Tongji University,Shanghai 200092,China

出　　处：《World Journal of Diabetes》2025年第4期19-24,共6页世界糖尿病杂志(英文)

基　　金：Supported by The Basic Research Project of Wenzhou Municipal Science and Technology Bureau,No.Y20240008;The Medical Health Science and Technology Project of Zhejiang Provincial Health Commission,No.2024KY138;The Key Laboratory of School of Laboratory Medicine and Life Sciences,Wenzhou Medical University of China,No.JS2023003。

摘　　要：In this editorial,we discussed the article published in the recent issue of the World Journal of Diabetes.To understand the effect of mizagliflozin on kidney injury induced by diabetes,we focused on the mechanisms by which high glucose triggers oxidative stress and contributes to kidney injury in diabetes.The high level of unmetabolized glucose reaching the kidney triggers glucose reabsorption by renal tubules,which elevates the cellular glucose level of renal cells.High glucose induces lactate dehydrogenase overexpression and thus shifts glucose metabolism,which causes mitochondrial dysfunction.Mitochondria generate approximately 90%of the reactive oxygen species in cells,whose dysfunction further alters glucose metabolism and enhances reactive oxygen species generation.Oxidative stress stimulates proinflammatory factor production and kidney inflammatory injury.Mizagliflozin decreases glucose reabsorption and thus ameliorates diabetes-induced kidney injury.

关 键 词：Glucose metabolism Sodium-D-glucose cotransporter 1 Glucose reabsorption Mitochondrial dysfunction Reactive oxygen species Inflammation 

分 类 号：R69[医药卫生—泌尿科学]