Journal
SEMINARS IN NEPHROLOGY
Volume 38, Issue 2, Pages 101-110Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semnephrol.2018.01.001
Keywords
Mitochondrial dysfunction; diabetic kidney disease; oxidative stress; hypoxia; uncoupling
Categories
Funding
- Australian Postgraduate Scholarships
- National Health and Medical Research Council [1089763, 100519]
- Heart Foundation Australia [1089763, 100519]
- NHMRC [1102935]
- National Health and Medical Research Council of Australia [1102935, 1089763] Funding Source: NHMRC
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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. (C) 2018 Elsevier Inc. All rights reserved.
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