ArticleIn vitro cellular & developmental biology. Animal2025
Atorvastatin inhibits ischemia‒reperfusion-associated renal tubular cell ferroptosis by blocking the PGE2/EP4 signaling pathway.
Article in In vitro cellular & developmental biology. Animal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Mitochondrial dysfunction-ferroptosis crosstalk drives renal fibrosis in chronic kidney disease.Renal failure · 2026Review
- Atorvastatin Attenuates Vancomycin-Induced Nephrotoxicity via PPARα-Associated Regulation of SLC Transporters.Drug design, development and therapy · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
Renal ischemia‒reperfusion (I/R) injury is the main cause of acute kidney injury, and its pathological features are manifested primarily by renal tubular epithelial cell injury. The underlying mechanism involves ferroptosis of renal tubular epithelial cells. Atorvastatin (ATO) regulates ferroptosis, and this study explored its role in I/R-induced ferroptosis of renal tubular epithelial cells. We constructed a renal I/R rat model with bilateral renal pedicles using noninvasive arterial clips and placed HK-2 cells in hypoxia/reoxygenation (H/R) incubators to construct the cell model. The damage to rat kidney tissues and HK-2 cells was assessed using enzyme-linked immunosorbent assay (ELISA), hematoxylin and eosin (H&E) staining, and flow cytometry, and the presence of associated proteins was identified through western blotting. Administering ATO markedly lessened the acute kidney damage caused by I/R, decreased the levels of blood urea nitrogen (BUN) and creatinine (CRE), and prevented apoptosis in renal tubular epithelial cells. Treatment with ATO additionally suppressed the production of inflammatory cytokines (TNF-α, IL-1β, and IL-6) and markers linked to ferroptosis (Fe
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