Journal article
Mitochondrial Dysfunction and Signaling in Diabetic Kidney Disease: Oxidative Stress and Beyond
Seminars in Nephrology, Vol.38(2), pp.101-110
2018
PMID: 29602393
Abstract
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.
Details
- Title
- Mitochondrial Dysfunction and Signaling in Diabetic Kidney Disease: Oxidative Stress and Beyond
- Authors
- Nicole Bernadette Flemming (Author) - University of QueenslandLinda A Gallo (Author) - University of QueenslandJosephine Maree Forbes (Author) - University of Melbourne
- Publication details
- Seminars in Nephrology, Vol.38(2), pp.101-110
- Publisher
- Elsevier Inc
- DOI
- 10.1016/j.semnephrol.2018.01.001
- ISSN
- 1558-4488
- PMID
- 29602393
- Organisation Unit
- School of Health and Behavioural Sciences - Legacy; University of the Sunshine Coast, Queensland; School of Health - Biomedicine
- Language
- English
- Record Identifier
- 99620607302621
- Output Type
- Journal article
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- Collaboration types
- Domestic collaboration
- Web Of Science research areas
- Urology & Nephrology
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Source: InCites