Mitochondria: a therapeutic target in acute kidney injury.
Acute kidney injury (AKI) is a common clinical entity that is associated with high mortality and morbidity. It is a risk factor for the development and progression of chronic kidney disease. Presently, no effective treatment for AKI is available, and novel therapeutic approaches are desperately needed. Accumulating evidence highlights mitochondrial dysfunction as an important factor in the pathogenesis of AKI. Recent advances in our understanding of the molecules involved in mitochondrial biogenesis, fusion/fission, mitophagy and their pathophysiological roles will lead to the development of drugs that target mitochondria for the treatment of various diseases, including AKI. In this review, we summarize current knowledge of the contribution of mitochondria-related pathophysiology in AKI and the prospective benefits of mitochondria-targeting therapeutic approaches against AKI.
Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Yu
Y
Ishimoto
Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan Division of Chronic Kidney Disease Pathophysiology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Reiko
R
Inagi
D058186:Acute Kidney Injury / Q000188:drug therapy* / Q000503:physiopathology; D000818:Animals; D006801:Humans; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004364:Pharmaceutical Preparations / Q000008:administration & dosage*
D004364:Pharmaceutical Preparations
acute kidney disease; mitochondrial biogenesis; mitochondrial fusion and fission; mitophagy; tubular damage