Mitochondrial Homeostasis in Acute Organ Failure

L. Jay Stallons, Jason A. Funk, Rick G. Schnellmann

Research output: Contribution to journalReview articlepeer-review

61 Scopus citations


The kidneys compose approximately 0.5 % of the body mass but consume about 10 % of the oxygen in cellular respiration. This discordance is due to the high energy demands on the kidney for reabsorption of filtered blood components and makes the kidney sensitive to stress on the mitochondria, the primary source of cellular ATP. Regardless of the etiology, acute kidney injury (AKI) almost always involves aspects of mitochondrial dysfunction. Recent evidence from experimental models suggests that preserving mitochondrial function or promoting mitochondrial repair rescues renal function during AKI. In this review we discuss the effect of AKI on disruption of mitochondrial homeostasis, and how the dynamic processes of mitochondrial biogenesis, fission/fusion, and mitophagy influence renal injury and recovery.

Original languageEnglish (US)
Pages (from-to)169-177
Number of pages9
JournalCurrent Pathobiology Reports
Issue number3
StatePublished - Sep 1 2013
Externally publishedYes


  • Acute kidney injury
  • Biogenesis
  • Dynamics
  • Mitochondria
  • Mitophagy
  • PGC-1α

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology
  • Cancer Research


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