DNA damage response in nephrotoxic and ischemic kidney injury

Mingjuan Yan, Chengyuan Tang, Zhengwei Ma, Shuang Huang, Zheng Dong

Research output: Contribution to journalReview articlepeer-review

52 Scopus citations


DNA damage activates specific cell signaling cascades for DNA repair, cell cycle arrest, senescence, and/or cell death. Recent studies have demonstrated DNA damage response (DDR) in experimental models of acute kidney injury (AKI). In cisplatin-induced AKI or nephrotoxicity, the DDR pathway of ATR/Chk2/p53 is activated and contributes to renal tubular cell apoptosis. In ischemic AKI, DDR seems more complex and involves at least the ataxia telangiectasia mutated (ATM), a member of the phosphatidylinositol 3-kinase-related kinase (PIKK) family, and p53; however, while ATM may promote DNA repair, p53 may trigger cell death. Targeting DDR for kidney protection in AKI therefore relies on a thorough elucidation of the DDR pathways in various forms of AKI.

Original languageEnglish (US)
Pages (from-to)104-108
Number of pages5
JournalToxicology and Applied Pharmacology
StatePublished - Dec 15 2016


  • Acute kidney injury
  • Cisplatin
  • DNA damage response
  • Renal ischemia/reperfusion

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology


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