ArticleScientific reports2025
Homocysteine induces ferroptosis in renal tubular epithelial cells via β-catenin/GPX4 signaling pathway.
Article in Scientific reports, 2025. 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.
- CB2R agonism protects intestinal epithelium through β-catenin/HoxA10 loop in radiation injury.Journal of translational medicine · 2026Article
- Population-scale characterization of the oral microbiome and associations with metabolic health.Nature communications · 2026Article
- Growth Differentiation Factor 15 (GDF15) Protects Against Sepsis-Associated Acute Kidney Injury via Suppression of TLR4-MyD88-NF-κB Signaling and Ferroptosis.BioFactors (Oxford, England)Article
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Authors and funding
6 authors.
Funding
Abstract
Hyperhomocysteinemia can cause severe damage to kidney. Ferroptosis represents a critical mechanism in the initiation and development of kidney disorders. We focus on the β-catenin/GPX4 signaling pathway to explore how homocysteine influences ferroptosis regulation in renal tubular epithelial cells. C57BL/6J mice were administered drinking water with high level of homocysteine to establish a hyperhomocysteinemia model. In the cell experiments, HKC-8 cells were exposed to homocysteine for a duration of 12 h. Active β-catenin, β-catenin, GPX4, FTH1, and KIM-1 were detected using Western blotting; Biochemical assays were conducted to measure lipid ROS, Fe
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