J Med Life Sci > Volume 15(2); 2018 > Article
Journal of Medicine and Life Science 2018;15(2):37-41.
DOI: https://doi.org/10.22730/jmls.2018.15.2.37    Published online January 3, 2019.
Mitochondrial fatty acid metabolism in acute kidney injury
Hee-Seong Jang, Babu Padanilam
University of Nebraska Medical Center
Correspondence:  Babu Padanilam, Email: bpadanilam@unmc.edu
Abstract
Mitochondrial injury in renal tubule has been recognized as a major contributor in acute kidney injury (AKI) pathogenesis. Ischemic insult, nephrotoxin, endotoxin and contrast medium destroy mitochondrial structure and function, as well as their biogenesis and dynamics, especially in renal proximal tubule, resulting in ATP depletion. Mitochondrial fatty acid oxidation (FAO) is the preferred source of ATP in the kidney, and its impairment is a critical factor in AKI pathogenesis. This review explores current knowledge of mitochondrial dysfunction and energy depletion in AKI and prospective views on developing therapeutic strategies targeting mitochondrial dysfunction in AKI.
Key Words: Mitochondria, energy, metabolism, fatty, acid
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