摘要
药物性肾损伤约占急性肾损伤发病率的20%,易发展为肾衰竭。目前临床除了肾脏替代疗法,尚无有效的治疗措施。越来越多的证据表明线粒体结构和功能损伤在药物性急性肾损伤的发生发展中发挥了重要作用。本文就药物性急性肾损伤领域中线粒体损伤的相关机制、潜在的生物标志物以及可能的干预靶点的研究进展作一综述,以期为临床上药物性急性肾损伤的早期诊断和治疗提供新的思路。
Drug-induced kidney injury accounts for roughly 20% of acute kidney injury（ AKI）,which is likely to progress into chronic renal failure.Currently,there are no available strategies except renal replacement therapy for drug-induced AKI.Accumulating evidence highlights mitochondrial structure abnormal and dysfunction contribute greatly to the onset and progression of drug-induced AKI.This review covers the research progress on the role of mitochondrial damage in drug-induced AKI,and also proposes potential biomarkers and intervention targets,which will provide new ideas for early diagnosis and treatment of drug-induced AKI.
作者
蔡名敏
姚澜
张经纬
周芳
王广基
CAI Mingmin;YAO Lan;ZHANG Jingwei;ZHOU Fang;WANG Guangji(Key Lab of Drug Metabolism and Pharmacokinetics , China Pharmaceutical University, Nanjing 210009, Jiangsu , China)
出处
《中国临床药理学与治疗学》
CAS
CSCD
2018年第5期578-585,共8页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
重大新药创制专项(2015ZX09501001
2017ZX09201001-006-005)
关键词
药物性急性肾损伤
线粒体损伤
肾毒性
drug-induced acute kidney injury
mitochondrial damage
nephrotoxicity
作者简介
蔡名敏，女，硕士研究生，研究方向：药物代谢动力学。Tel：15250962898E—mail：mingmincai@163．com;王广基，通信作者，男，中国工程院院士，教授，博士生导师，研究方向：药物代谢动力学。Tel：025-83271128E-mail：guangjiwang@hotmail．com
