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      Mitochondrial dysfunction in kidney injury, inflammation, and disease: potential therapeutic approaches

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          Abstract

          Mitochondria are energy-producing organelles that not only satisfy the high metabolic demands of the kidney but sense and respond to kidney injury-induced oxidative stress and inflammation. Kidneys are rich in mitochondria. Mitochondrial dysfunction plays a critical role in the progression of acute kidney injury and chronic kidney disease. Mitochondrial responses to specific stimuli are highly regulated and synergistically modulated by tightly interconnected processes, including mitochondrial dynamics (fission, fusion) and mitophagy. The counterbalance between these processes is essential in maintaining a healthy network of mitochondria. Recent literature suggests that alterations in mitochondrial dynamics are implicated in kidney injury and the progression of kidney diseases. A decrease in mitochondrial fusion promotes fission-induced mitochondrial fragmentation, but a reduction in mitochondrial fission produces excessive mitochondrial elongation. The removal of dysfunctional mitochondria by mitophagy is crucial for their quality control. Defective mitochondrial function disrupts cellular redox potential and can cause cell death. Mitochondrial DNA derived from damaged cells also act as damage-associated molecular patterns to recruit immune cells and the inflammatory response can further exaggerate kidney injury. This review provides a comprehensive overview of the role of mitochondrial dysfunction in acute kidney injury and chronic kidney disease. We discuss the processes that control mitochondrial stress responses to kidney injury and review recent advances in understanding the role of mitochondrial dysfunction in inflammation and tissue damage through the use of different experimental models of kidney disease. We also describe potential mitochondria-targeted therapeutic approaches.

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          Mechanisms of Cisplatin Nephrotoxicity

          Cisplatin is a widely used and highly effective cancer chemotherapeutic agent. One of the limiting side effects of cisplatin use is nephrotoxicity. Research over the past 10 years has uncovered many of the cellular mechanisms which underlie cisplatin-induced renal cell death. It has also become apparent that inflammation provoked by injury to renal epithelial cells serves to amplify kidney injury and dysfunction in vivo. This review summarizes recent advances in our understanding of cisplatin nephrotoxicity and discusses how these advances might lead to more effective prevention.
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            Mitochondrial energetics in the kidney

            Mitochondria provide the kidney with energy to remove waste from the blood and regulate fluid and electrolyte balance. This Review discusses how mitochondrial homeostasis is maintained, the changes in mitochondrial energetics that occur in acute kidney injury and diabetic nephropathy, and how targeting mitochondrial energetics might aid the treatment of renal disease.
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              Mitochondrial dynamics and inheritance during cell division, development and disease.

              During cell division, it is critical to properly partition functional sets of organelles to each daughter cell. The partitioning of mitochondria shares some common features with that of other organelles, particularly in the use of interactions with cytoskeletal elements to facilitate delivery to the daughter cells. However, mitochondria have unique features - including their own genome and a maternal mode of germline transmission - that place additional demands on this process. Consequently, mechanisms have evolved to regulate mitochondrial segregation during cell division, oogenesis, fertilization and tissue development, as well as to ensure the integrity of these organelles and their DNA, including fusion-fission dynamics, organelle transport, mitophagy and genetic selection of functional genomes. Defects in these processes can lead to cell and tissue pathologies.
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                Author and article information

                Journal
                Kidney Res Clin Pract
                Kidney Research and Clinical Practice
                Korean Society of Nephrology
                2211-9132
                2211-9140
                30 September 2020
                30 September 2020
                : 39
                : 3
                : 244-258
                Affiliations
                [1 ]Division of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, New York, NY, USA
                [2 ]Department of Medicine, NewYork-Presbyterian Hospital/Weill Cornell Medicine, New York, NY, USA
                Author notes
                Correspondence: Mary E. Choi, Division of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, 525 East 68th Street, Box 3, New York, NY 10065, USA. E-mail: mechoi@ 123456med.cornell.edu

                Editor: Gheun-Ho Kim, Hanyang University, Seoul, Republic of Korea

                Author information
                https://orcid.org/0000-0002-8236-3440
                https://orcid.org/0000-0003-0557-273X
                https://orcid.org/0000-0002-6853-336X
                Article
                KRCP-39-244
                10.23876/j.krcp.20.082
                7530368
                32868492
                cfd6c656-d652-4f0d-b039-8dc42eaeb914
                Copyright © 2020 by The Korean Society of Nephrology

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 May 2020
                : 21 June 2020
                : 23 June 2020
                Categories
                Review Article

                acute kidney injury,inflammation,kidney diseases,mitochondria,oxidative stress

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