Format

Send to

Choose Destination
Semin Nephrol. 2018 Mar;38(2):101-110. doi: 10.1016/j.semnephrol.2018.01.001.

Mitochondrial Dysfunction and Signaling in Diabetic Kidney Disease: Oxidative Stress and Beyond.

Author information

1
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.
2
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.

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.

KEYWORDS:

Mitochondrial dysfunction; diabetic kidney disease; hypoxia; oxidative stress; uncoupling

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center