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Kidney Int. 2017 Nov;92(5):1051-1057. doi: 10.1016/j.kint.2017.05.034.

The hallmarks of mitochondrial dysfunction in chronic kidney disease.

Author information

1
Section of Nephrology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
2
Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas, USA.
3
Section of Nephrology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA; Department of Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas, USA. Electronic address: fdanesh@mdanderson.org.

Abstract

Recent advances have led to a greater appreciation of how mitochondrial dysfunction contributes to diverse acute and chronic pathologies. Indeed, mitochondria have received increasing attention as a therapeutic target in a variety of diseases because they serve as key regulatory hubs uniquely situated at crossroads between multiple cellular processes. This review provides an overview of the role of mitochondrial dysfunction in chronic kidney disease, with special emphasis on its role in the development of diabetic nephropathy. We examine the current understanding of the molecular mechanisms that cause mitochondrial dysfunction in the kidney and describe the impact of mitochondrial damage on kidney function. The new concept that mitochondrial shape and structure are closely linked with its function in the kidneys is discussed. Furthermore, the mechanisms that translate cellular cues and demands into mitochondrial remodeling and cellular damage, including the role of microRNAs and long noncoding RNAs, are examined with the final goal of identifying mitochondrial targets to improve treatment of patients with chronic kidney diseases.

KEYWORDS:

acute kidney injury; chronic kidney disease; diabetes; diabetic nephropathy; mitochondria; oxidative stress

PMID:
28893420
PMCID:
PMC5667560
DOI:
10.1016/j.kint.2017.05.034
[Indexed for MEDLINE]
Free PMC Article

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