Peroxisomes and Kidney Injury

Antioxid Redox Signal. 2016 Aug 1;25(4):217-31. doi: 10.1089/ars.2016.6666. Epub 2016 Apr 22.


Significance: Peroxisomes are organelles present in most eukaryotic cells. The organs with the highest density of peroxisomes are the liver and kidneys. Peroxisomes possess more than fifty enzymes and fulfill a multitude of biological tasks. They actively participate in apoptosis, innate immunity, and inflammation. In recent years, a considerable amount of evidence has been collected to support the involvement of peroxisomes in the pathogenesis of kidney injury.

Recent advances: The nature of the two most important peroxisomal tasks, beta-oxidation of fatty acids and hydrogen peroxide turnover, functionally relates peroxisomes to mitochondria. Further support for their communication and cooperation is furnished by the evidence that both organelles share the components of their division machinery. Until recently, the majority of studies on the molecular mechanisms of kidney injury focused primarily on mitochondria and neglected peroxisomes.

Critical issues: The aim of this concise review is to introduce the reader to the field of peroxisome biology and to provide an overview of the evidence about the contribution of peroxisomes to the development and progression of kidney injury. The topics of renal ischemia-reperfusion injury, endotoxin-induced kidney injury, diabetic nephropathy, and tubulointerstitial fibrosis, as well as the potential therapeutic implications of peroxisome activation, are addressed in this review.

Future directions: Despite recent progress, further studies are needed to elucidate the molecular mechanisms induced by dysfunctional peroxisomes and the role of the dysregulated mitochondria-peroxisome axis in the pathogenesis of renal injury. Antioxid. Redox Signal. 25, 217-231.

Publication types

  • Review

MeSH terms

  • Animals
  • Autophagy
  • Disease Models, Animal
  • Fatty Acids / metabolism
  • Homeostasis
  • Humans
  • Kidney / metabolism*
  • Kidney Diseases / etiology*
  • Kidney Diseases / metabolism*
  • Oxidation-Reduction
  • Oxidative Stress
  • Peroxisomes / metabolism*
  • Reactive Oxygen Species / metabolism


  • Fatty Acids
  • Reactive Oxygen Species