Molecular mechanisms of ischemic preconditioning in the kidney

Pinelopi P. Kapitsinou*, Volker H. Haase

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

43 Scopus citations

Abstract

More effective therapeutic strategies for the prevention and treatment of acute kidney injury (AKI) are needed to improve the high morbidity and mortality associated with this frequently encountered clinical condition. Ischemic and/or hypoxic preconditioning attenuates susceptibility to ischemic injury, which results from both oxygen and nutrient deprivation and accounts for most cases of AKI. While multiple signaling pathways have been implicated in renoprotection, this review will focus on oxygen-regulated cellular and molecular responses that enhance the kidney’s tolerance to ischemia and promote renal repair. Central mediators of cellular adaptation to hypoxia are hypoxia-inducible factors (HIFs). HIFs play a crucial role in ischemic/hypoxic preconditioning through the reprogramming of cellular energy metabolism, and by coordinating adenosine and nitric oxide signaling with antiapoptotic, oxidative stress, and immune responses. The therapeutic potential of HIF activation for the treatment and prevention of ischemic injuries will be critically examined in this review.

Original languageEnglish (US)
Pages (from-to)F821-F834
JournalAmerican Journal of Physiology - Renal Physiology
Volume309
Issue number10
DOIs
StatePublished - 2015

Keywords

  • Acute kidney injury
  • Adenosine
  • Dioxygenases
  • Erythropoietin
  • HIF prolyl-4-hydroxylases
  • Hypoxia
  • Hypoxia-inducible factor
  • Inflammation
  • Ischemic preconditioning
  • Oxygen sensing

ASJC Scopus subject areas

  • Physiology
  • Urology

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