ArticleMolecular biology reports2026
OLFM4 mediating ischemia/reperfusion-induced kidney injury by regulating renal tubular epithelial cells ferroptosis via GPX4.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Multidimensional targeting of ischemia-reperfusion injury by genistein: from molecular crosstalk to clinical translation.Frontiers in pharmacology · 2026Review
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Abstract
backgroundIschemia-reperfusion acute kidney injury (IRI-AKI) is a common critical clinical condition characterized by high morbidity and mortality. Renal tubular epithelial cells (TECs) ferroptosis plays a key role in the pathogenesis of IRI-AKI. We observed that olfactomedin 4 (OLFM4) expressed in TECs and was downregulated in the kidney of AKI patients. And the downregulation of OLFM4 was correlated with TECs ferroptosis. Therefore, our present study intended to clarify the role and mechanism of OLFM4 in TEC ferroptosis and IRI-AKI.
methodsOLFM4-deficient HK-2 cell lines and OLFM4−/− mice were generated. In vitro hypoxia/reoxygenation (H/R) TECs model and IRI-AKI mouse models, were employed. Renal injury and ferroptosis-related markers were evaluated by immunofluorescence, Western blotting, and biochemical assays to evaluate the role of OLFM4 in TECs ferroptosis. Molecular docking, co-immunoprecipitation (Co-IP), and yeast two-hybrid assays were performed to identify the mechanism of OLFM4 on ferroptosis pathway.
resultsOLFM4 was markedly downregulated in renal tissues of IRI-AKI mice and HK-2 cells subjected to H/R. OLFM4 deficiency aggravated renal function impairment of the IRI-AKI mice (Cr, BUN), accompanied by elevated ferroptosis markers (Fe²⁺, ROS, and MDA) and reduced GSH, whereas OLFM4 overexpression ameliorated IRI-AKI and suppressed TECs ferroptosis. Additionally, we demonstrated that OLFM4 stabilizes GPX4 by inhibiting its ubiquitination, and GPX4 is a key molecule in the occurrence of ferroptosis. The overexpression of OLFM4 upregulating GPX4 expression, enhancing antioxidant defenses, and attenuating TECs ferroptosis in H/R HK-2 cell model and IRI-AKI mice.
conclusionsOur present study demonstrates that OLFM4 reduction play an important role in IRI-AKI occurrence. Overexpression could protect IRI-AKI by reducing TEC ferroptosis via GPX4. For the first time, OLFM4 is identified as a ferroptosis suppressor, expanding our understanding of AKI pathogenesis, and highlighting OLFM4 as a potential therapeutic target.
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