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Technical Refinement of a Bilateral Renal Ischemia-Reperfusion Mouse Model for Acute Kidney Injury Research
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Research progress of ferroptosis in acute kidney injury

Lin Zhang1, Feng Luo2, Nan Yuan1

  • 1Department of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.

Frontiers in Cell and Developmental Biology
|July 10, 2025
PubMed

Insights

Ferroptosis, a cell death process, is increasingly linked to acute kidney injury (AKI). Inhibiting ferroptosis shows promise for treating AKI, though its exact role needs further study.

Area of Science:

  • Nephrology
  • Cellular Biology
  • Biochemistry

Background:

  • Acute kidney injury (AKI) is a critical condition with limited treatment options.
  • Ferroptosis, an iron-dependent cell death pathway involving lipid peroxidation, is implicated in AKI pathogenesis.
  • Elevated ferroptosis markers are observed in various AKI models, suggesting its contribution to kidney damage.

Purpose of the Study:

  • To review the current understanding of ferroptosis in the context of AKI.
  • To elucidate the molecular mechanisms regulating ferroptosis in kidney injury.
  • To identify potential therapeutic targets for AKI based on ferroptosis inhibition.

Main Methods:

  • Literature review of studies investigating ferroptosis and AKI.
  • Analysis of molecular pathways involved in ferroptosis.
  • Examination of ferroptosis markers in different AKI types.

Main Results:

  • Ferroptosis is involved in AKI caused by ischemia-reperfusion, sepsis, nephrotoxic agents, and rhabdomyolysis.
  • Inhibition of ferroptosis has demonstrated protective effects in experimental AKI models.
  • Specific regulatory mechanisms of ferroptosis in AKI require further investigation.

Conclusions:

  • Ferroptosis is a significant contributor to AKI across various etiologies.
  • Targeting ferroptosis presents a promising therapeutic avenue for AKI.
  • Further research into ferroptosis regulation is crucial for developing effective AKI interventions.
Keywords:
acute kidney injuryferroptosislipid peroxidationmechanismstherapeutic targets

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