ArticleJournal of advanced research2026
Squalene epoxidase promotes paraquat-induced pulmonary toxicity through endoplasmic reticulum-mediated ferroptosis.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Pesticides Drive Liver Diseases Through Non-Apoptotic Regulated Cell Death Pathways.Diseases (Basel, Switzerland) · 2026Review
- SIRT6 Relieves Acute Lung Injury by Enhancing PGC-1α Expression and Improving Mitochondrial Function.Current molecular medicine · 2026Article
- Ferroptosis in diabetic retinopathy: from pathogenic mechanisms to translational prospects.Frontiers in endocrinology · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
introductionParaquat (PQ), a widely used herbicide, causes lethal lung injury through unresolved mechanisms, posing urgent clinical challenges due to the lack of effective antidotes.
objectivesThis study aimed to define the role of squalene epoxidase (SQLE) in PQ-induced ferroptosis and endoplasmic reticulum (ER) stress, and to evaluate the therapeutic efficacy of the SQLE inhibitor liranaftate (LNT).
methodsCytotoxicity was assessed via CCK-8, ATP assays, and PI staining. Labile iron levels and lipid peroxidation were quantified using flow cytometry. ER morphology was visualized with ER-Tracker Green, mitochondrial swelling with MitoTracker Green, and ferrous iron localization with FerroOrange Live Cell Dye. Iron donors (FeSO
resultsPQ triggered ferroptosis via ER stress-dependent PERK/eIF2α activation, with SQLE identified as a key mediator. LNT suppressed PQ-induced cytotoxicity by reducing labile iron, lipid peroxidation, and ER/mitochondrial damage. Iron supplementation exacerbated ferroptosis, while LNT restored GPX4 and SLC7A11 expression. In vivo, LNT treatment significantly improved survival rates from 45% in the PQ model group to 95%, while attenuating ALI severity by blocking the PERK signaling pathway and upregulating the ferroptosis-related proteins GPX4 and SLC7A11.
conclusionThese findings highlight the potential role of ferroptosis and SQLE in mediating PQ toxicity and provide therapeutic strategies to combat PQ toxicity by inhibiting ferroptosis and/or targeting SQLE. Repurposing LNT may be a potential antidote for PQ-induced ALI.
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