Mitochondrial Dysfunction and Signaling in Diabetic Kidney Disease: Oxidative Stress and Beyond.
Autor: | Flemming NB; Glycation and Diabetes Group, Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, Queensland, Australia; School of Biomedical Sciences, The University of Queensland, St Lucia, Queensland, Australia., Gallo LA; Glycation and Diabetes Group, Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, Queensland, Australia; School of Biomedical Sciences, The University of Queensland, St Lucia, Queensland, Australia., Forbes JM; Glycation and Diabetes Group, Mater Research Institute, The University of Queensland, Translational Research Institute, Woolloongabba, Queensland, Australia; Department of Medicine, The University of Melbourne, Melbourne, Victoria, Heidelberg, Australia. Electronic address: josephine.forbes@mater.uq.edu.au. |
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Jazyk: | angličtina |
Zdroj: | Seminars in nephrology [Semin Nephrol] 2018 Mar; Vol. 38 (2), pp. 101-110. |
DOI: | 10.1016/j.semnephrol.2018.01.001 |
Abstrakt: | The kidneys are highly metabolic organs that produce vast quantities of adenosine triphosphate via oxidative phosphorylation and, as such, contain many mitochondria. Although mitochondrial reactive oxygen species are involved in many physiological processes in the kidneys, there is a plethora of evidence to suggest that excessive production may be a pathologic mediator of many chronic kidney diseases, including diabetic kidney disease. Despite this, results from clinical testing of antioxidant therapies have been generally underwhelming. However, given the many roles of mitochondria in cellular functioning, pathways other than reactive oxygen species production may prevail as pathologic mediators in diabetic kidney disease. Accordingly, in this review, mitochondrial dysfunction in a broader context is discussed, specifically focusing on mitochondrial respiration and oxygen consumption, intrarenal hypoxia, oxidative stress, mitochondrial uncoupling, and networking. (Copyright © 2018 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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