Dephosphorylation of AMP-activated protein kinase exacerbates ischemia/reperfusion-induced acute kidney injury via mitochondrial dysfunction.

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作者： Haijian,Ma ^[1] ; Xiaozhen,Guo ^[2] ; Shichao,Cui ^[2] ; Yongmei,Wu ^[3] ; Yangming,Zhang ^[4] ; Xiaoyan,Shen ^[5] ; Cen,Xie ^[6] ; Jingya,Li ^[7]

作者单位： Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China. ^[1] State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China. ^[2] School of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, China. ^[3] State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China; Yantai Key Laboratory of Nanomedicine and Advanced Preparations, Yantai Institute of Materia Medica, Shandong, China. ^[4] Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai, China. Electronic address: shxiaoy@fudan.edu.cn. ^[5] State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China. Electronic address: xiecen@simm.ac.cn. ^[6] State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China; School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, Chinese Academy of Sciences, Hangzhou, China. Electronic address: jyli@simm.ac.cn. ^[7]

关键词 AMPK acute kidney injury autophagy lipid metabolism mitochondrial biogenesis