ArticleMolecular medicine reports2022
Ferrostatin‑1 alleviates oxalate‑induced renal tubular epithelial cell injury, fibrosis and calcium oxalate stone formation by inhibiting ferroptosis.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Dysregulated iron metabolism and kidney stone risk: an epidemiological and experimental study.Renal failure · 2026Article
- Bufalin post-transcriptionally suppresses STAT3 to alleviate renal ferroptosis and tubulointerstitial fibrosis in diabetic kidney disease.Renal failure · 2026Article
- Phenylalanine primes renal tubular redox vulnerability and calcium oxalate crystal retention through a PPARδ-CPT1A fatty-acid oxidation axis.Redox biology · 2026Article
- Possible role of ribosome biogenesis in the recovery from transient hepatic damage caused by ethylene glycol in rats.Forensic toxicology · 2026Article
- Azilsartan as a novel anti-ferriptotic agent via the upregulation of the Nrf2/HO-1/SLC7A11/GPX4 axis and downregulation of inflammatory pathways in folic acid-induced acute kidney injury in male mice.Toxicology reports · 2026Article
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- Small molecules targeting regulated cell death for chronic kidney disease therapy.Journal of pharmaceutical analysis · 2026Review
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- <p>Pathological mechanism of ferroptosis in a rat model of α‑naphthyl isothiocyanate‑induced chronic cholestasis</p>.Molecular medicine reports · 2026Article
- Machine learning-driven multi-omics integration of urinary organic acids and ions enables precision risk stratification for calcium oxalate nephrolithiasis.Frontiers in medicine · 2026Article
- Regulated Cell Death in Calcium Oxalate Stone Disease: From Tubular Epithelial Injury to Inflammatory Amplification.Journal of inflammation research · 2026Review
- GGT1 protects against calcium oxalate crystal-induced renal tubular epithelial cell injury by targeting GCLC.Urolithiasis · 2025Article
- HPDA-based tubule-targeting nanoplatform alleviates oxidative stress and ferroptosis for the reversal of renal interstitial fibrosis.Journal of nanobiotechnology · 2025Article
- 5'tiRNA-Glu-TTC targets TRPV3 and activates the PI3K/AKT signaling pathway to modulate skin photoaging.Non-coding RNA research · 2025Article
- Linoelaidic acid alleviates COM-induced kidney injury and crystal deposition via the PPARγ/MAPK signaling pathway.Urolithiasis · 2025Article
- Apoptosis, ferroptosis, necrosis, necroptosis and pyroptosis in the formation of calcium oxalate kidney stones.Urolithiasis · 2025Review
- Ferroptosis: A key regulator and potential target for tissue injury.Histology and histopathology · 2025Review
- Hepatic ferroptosis induced by Clonorchis sinensis exacerbates liver fibrosis.PLoS neglected tropical diseases · 2025Article
- Mitochondrial SLC3A1 regulates sexual dimorphism in cystinuria.Genes & diseases · 2025Article
- SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.Aging and disease · 2025Review
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7 authors.
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Abstract
The present study aimed to evaluate the role and mechanism of ferrostatin‑1 (Fer‑1) in oxalate (Ox)‑induced renal tubular epithelial cell injury, fibrosis, and calcium oxalate (CaOx) stone formation. A CaOx model in mice kidneys was established via intraperitoneal injection of 80 mg/kg glyoxylic acid for 14 days. The mice were randomly divided into three groups (n=6), namely, the control (Con), the CaOx group, and the CaOx + Fer‑1 group. Cultured human renal tubular epithelial cells (HK‑2 cells) were randomly divided into three groups (n=3), namely, the control (Con), the Ox group, and the Ox + Fer‑1 group. The levels of heme oxygenase 1 (HO‑1), superoxide dismutase 2 (SOD2), glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 (SLC7A11) were assessed by immunofluorescence and western blot analysis. Renal tubular injury and apoptosis were evaluated by H&E and TUNEL staining. Kidney interstitial fibrosis was evaluated by Masson and Sirius red staining, and the levels of E‑cadherin, vimentin and α‑SMA were detected by immunofluorescence or western blot analysis. Mitochondrial structure was observed using a transmission electron microscope. The levels of reactive oxygen species (ROS) were determined by flow cytometry and CaOx stone formation was evaluated by von Kossa staining. The results revealed that in comparison with the Con group, mitochondrial injury under glyoxylic acid treatment was observed by TEM. The expression of GPX4 and SLC7A11 in the CaOx and Ox groups was downregulated (P<0.05), whereas the expression of HO‑1 and SOD2 was upregulated (P<0.05). Renal tissue damage, apoptosis of renal tubular epithelial cells, and interstitial fibrosis were increased in the CaOx and Ox groups (P<0.05). In comparison with the CaOx or Ox group, the expression of GPX4 and SLC7A11 in the CaOx + Fer‑1 or Ox + Fer‑1 group was upregulated (P<0.05), whereas that of HO‑1 and SOD2 was downregulated (P<0.05). Renal tissue damage, apoptosis of renal tubular epithelial cells and interstitial fibrosis were decreased following Fer‑1 treatment (P<0.05). The ROS level was also decreased following Fer‑1 treatment. Moreover, CaOx stone formation was decreased in the CaOx + Fer‑1 group (P<0.05). In conclusion, Fer‑1 alleviated Ox‑induced renal tubular epithelial cell injury, fibrosis, and CaOx stone formation by inhibiting ferroptosis.
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