Ablation of peroxiredoxin v exacerbates ischemia/reperfusion-induced kidney injury in mice

Jiyoung Park, Eun Gyeong Lee, Ho Jin Yi, Nam Hee Kim, Sue Goo Rhee, Hyun Ae Woo

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Ischemia/reperfusion (I/R) is one of the major causes of acute kidney injury (AKI) and associated with increased mortality and progression to chronic kidney injury (CKI). Molecular mechanisms underlying I/R injury involve the production and excessive accumulation of reactive oxygen species (ROS). Peroxiredoxin (Prx) V, a cysteine-dependent peroxidase, is located in the cytosol, mitochondria, and peroxisome and has an intensive ROS scavenging activity. Therefore, we focused on the role of Prx V during I/R-induced AKI using Prx V knockout (KO) mice. Ablation of Prx V augmented tubular damage, apoptosis, and declined renal function. Prx V deletion also showed higher susceptibility to I/R injury with increased markers for oxidative stress, ER stress, and inflammation in the kidney. Overall, these results demonstrate that Prx V protects the kidneys against I/R-induced injury.

Original languageEnglish
Article number769
Pages (from-to)1-12
Number of pages12
Issue number8
StatePublished - Aug 2020

Bibliographical note

Publisher Copyright:
© 2020 by the authors. Licensee MDPI, Basel, Switzerland.


  • Peroxiredoxin V
  • Reactive oxygen species
  • Renal dysfunction
  • Renal ischemia/reperfusion


Dive into the research topics of 'Ablation of peroxiredoxin v exacerbates ischemia/reperfusion-induced kidney injury in mice'. Together they form a unique fingerprint.

Cite this