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KMID : 1161920180150020037
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Journal of Medicine and Life Science
2018 Volume.15 No. 2 p.37 ~ p.41
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Mitochondrial fatty acid metabolism in acute kidney injury
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Jang Hee-Seong
Padanilam Babu J.
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Abstract
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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.
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KEYWORD
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Mitochondria, Energy metabolism, Fatty acid oxidation, ATP, Mitochondrial dysfunction, Ischemia/reperfusion injury, Nephrotoxin, Sepsis, Acute kidney injury
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