Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases

Hee Seong Jang, Mi Ra Noh, Jinu Kim, Babu J. Padanilam

Research output: Contribution to journalReview articlepeer-review

91 Scopus citations


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.

Original languageEnglish (US)
Article number65
JournalFrontiers in Medicine
StatePublished - Mar 12 2020


  • acute kidney injury
  • chronic kidney disease
  • diabetic nephropathy
  • fatty acid β-oxidation
  • glomerular nephropathy
  • lipotoxicity
  • mitochondria
  • polycystic kidney disease

ASJC Scopus subject areas

  • General Medicine


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