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...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in medicine Vol. 7; p. 65
Main Authors Jang, Hee-Seong, Noh, Mi Ra, Kim, Jinu, Padanilam, Babu J
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 12.03.2020
Subjects
Online AccessGet full text

Cover

Loading…
More Information
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.
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