ArticleJournal of diabetes investigation2025
Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway.
Article in Journal of diabetes investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The miR-145-5p/NRF2/SLC7A11 axis regulates ferroptosis-mediated renal tubular epithelial cell injury in diabetic nephropathy.Journal of diabetes investigation · 2026Article
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- Research progress of cuproptosis, ferroptosis, apoptosis, and autophagy in knee osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Cordycepin nephroprotection: From STZ mouse to human T2D.Journal of diabetes investigation · 2025Article
- Review
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- High glucose-induced PLCG1 histone acetylation to promote ferroptosis by LAMP2A/HSPA8 in a diabetic nephropathy model.Frontiers in pharmacology · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundCordycepin (CRD) has been identified to alleviate diabetes-induced injuries and complications including diabetic nephropathy (DN). Here, this work focused on probing the specific effects and potential mechanisms of CRD on DN progression.
methodsHigh glucose (HG)-induced mouse podocyte cell line (MPC5) was used for in vitro functional analyses. Cell proliferation and apoptosis were determined using cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine assay, and flow cytometry, respectively. ELISA analysis detected inflammatory factors. Cell ferroptosis was assessed by measuring the levels of Fe2+, glutathione, reactive oxygen species, and malonaldehyde.
resultsCRD treatment suppressed HG-induced apoptosis, inflammation, and ferroptosis in podocytes. CRD treatment elevated SLC7A11 and GPX4 expression in HG-treated podocytes. The overexpression of SLC7A11 or GPX4 suppressed HG-evoked apoptosis, inflammation, and ferroptosis in podocytes. Moreover, the silencing of SLC7A11 or GPX4 abolished the protective effects of CRD on HG-treated podocytes. Moreover, CRD ameliorated renal structure injury and inflammation in STZ-induced diabetic mice by modulating SLC7A11 or GPX4 expression.
conclusionsCordycepin suppressed HG-induced apoptosis, inflammation, and ferroptosis in podocytes in vitro, and ameliorated renal injury and inflammation in STZ-induced diabetic mice by activating the SLC7A11/GPX4 pathway.
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