ArticleThe Journal of clinical investigation2019
Myo-inositol oxygenase expression profile modulates pathogenic ferroptosis in the renal proximal tubule.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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Who cites it
121 citing papers in PubMed, 215 citations in OpenAlex.
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Regulation of Glutathione Peroxidase 4 in Diabetic Retinopathy.International journal of molecular sciences · 2026Article
- Review
- Erythropoietin and Ferulic Acid Loaded on FeApplied biochemistry and biotechnology · 2026Article
- Icariin protects against cisplatin-induced renal injury and ferroptosis via JNK pathway in mice.BMC nephrology · 2026Article
- Phenothiazine alleviates cisplatin-mediated acute kidney injury by inhibiting ferroptosis.Cell and tissue research · 2026Article
- Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis.Chinese medicine · 2026Article
- Keratin 20 Suppresses Exosomal Secretion of Peroxiredoxin 2 and Ferroptosis in Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026Article
- TET2: a critical regulatory hub with broad therapeutic implications across human diseases.Frontiers in immunology · 2026Review
- Ferroptosis: A Double-Edged Sword in Cisplatin-Based Cancer Therapy and Acute Kidney Injury.Cancer management and research · 2026Review
- Targeting mitochondrial damage and ER stress to inhibit ferroptosis in cadmium-induced nephrotoxicity.Toxicology reports · 2025Review
- The Role of Ubiquitination and Deubiquitination in the Pathogenesis of Acute Kidney Injury: Progress in Research.Biomedicines · 2025Review
- Verbenalin attenuates renal tubular epithelial ferroptosis in ischemia-reperfusion injury induced AKI by regulating the HIF-1α/HO-1 signaling pathway.BMC nephrology · 2025Article
- SELENBP1 protects against kidney fibrosis in chronic kidney disease as a methanethiol oxidase.Science China. Life sciences · 2025Article
- Myo-Inositol Oxygenase (MIOX): A Pivotal Regulator and Therapeutic Target in Multiple Diseases.Current issues in molecular biology · 2025Review
- Acute kidney injury: pathogenesis and therapeutic interventions.Molecular biomedicine · 2025Review
- Ferroptosis in Cancer and Inflammatory Diseases: Mechanisms and Therapeutic Implications.MedComm · 2025Review
- The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis.Nature communications · 2025Article
- miR-4537 curtails ferroptosis by targeting MIOX in renal cell carcinoma.Translational oncology · 2025Article
- Integrated analysis of MIOX gene in prognosis of clear-cell renal cell carcinoma.Cell death & disease · 2025Article
61 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Overexpression of myo-inositol oxygenase (MIOX), a proximal tubular enzyme, exacerbates cellular redox injury in acute kidney injury (AKI). Ferroptosis, a newly coined term associated with lipid hydroperoxidation, plays a critical role in the pathogenesis of AKI. Whether or not MIOX exacerbates tubular damage by accelerating ferroptosis in cisplatin-induced AKI remains elusive. Cisplatin-treated HK-2 cells exhibited notable cell death, which was reduced by ferroptosis inhibitors. Also, alterations in various ferroptosis metabolic sensors, including lipid hydroperoxidation, glutathione peroxidase 4 (GPX4) activity, NADPH and reduced glutathione (GSH) levels, and ferritinophagy, were observed. These perturbations were accentuated by MIOX overexpression, while ameliorated by MIOX knockdown. Likewise, cisplatin-treated CD1 mice exhibited tubular damage and derangement of renal physiological parameters, which were alleviated by ferrostatin-1, a ferroptosis inhibitor. To investigate the relevance of MIOX to ferroptosis, WT mice, MIOX-overexpressing transgenic (MIOX-Tg) mice, and MIOX-KO mice were subjected to cisplatin treatment. In comparison with cisplatin-treated WT mice, cisplatin-treated MIOX-Tg mice had more severe renal pathological changes and perturbations in ferroptosis metabolic sensors, which were minimal in cisplatin-treated MIOX-KO mice. In conclusion, these findings indicate that ferroptosis, an integral process in the pathogenesis of cisplatin-induced AKI, is modulated by the expression profile of MIOX.
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