Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases
The kidney is a highly metabolic organ and uses high levels of ATP to maintain electrolyte and acid-base homeostasis and reabsorb nutrients. Energy depletion is a critical factor in development and progression of various kidney diseases including acute kidney injury (AKI), chronic kidney disease (CK...
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Published in | Frontiers in medicine Vol. 7; p. 65 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
12.03.2020
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Subjects | |
Online Access | Get full text |
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Summary: | The kidney is a highly metabolic organ and uses high levels of ATP to maintain electrolyte and acid-base homeostasis and reabsorb nutrients. Energy depletion is a critical factor in development and progression of various kidney diseases including acute kidney injury (AKI), chronic kidney disease (CKD), and diabetic and glomerular nephropathy. Mitochondrial fatty acid β-oxidation (FAO) serves as the preferred source of ATP in the kidney and its dysfunction results in ATP depletion and lipotoxicity to elicit tubular injury and inflammation and subsequent fibrosis progression. This review explores the current state of knowledge on the role of mitochondrial FAO dysfunction in the pathophysiology of kidney diseases including AKI and CKD and prospective views on developing therapeutic interventions based on mitochondrial energy metabolism. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 Edited by: John D. Imig, Medical College of Wisconsin, United States This article was submitted to Nephrology, a section of the journal Frontiers in Medicine Reviewed by: Jonatan Barrera-Chimal, National Autonomous University of Mexico, Mexico; Kirk Campbell, Icahn School of Medicine at Mount Sinai, United States |
ISSN: | 2296-858X 2296-858X |
DOI: | 10.3389/fmed.2020.00065 |