ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Irisin attenuates tubular epithelial ferroptosis in diabetic kidney disease by inhibiting the HMGB1/Nrf2/GPX4 pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 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.
- Shengqingjiangzhuo Capsules Alleviates Renal Fibrosis by Targeting Glomerular Endothelial Cells Exosome miR-31-5p/HO-1 to Suppress Tubular Epithelial Cells Ferroptosis.Clinical and experimental pharmacology & physiology · 2026Article
- HMGB1: a key molecule linking chronic inflammation to complications in type 2 diabetes mellitus and a target for exercise intervention.Frontiers in endocrinology · 2026Review
- Relationship between serum glucose-to-albumin ratio and kidney stones among nondiabetic U.S. adults: a population-based study.Translational andrology and urology · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Diabetic nephropathy (DN) is a global health threat with limited therapeutic interventions. Irisin, a myokine derived from FNDC5, has been implicated in glucose homeostasis and anti-diabetic effects; however, its precise mechanistic role in glucose metabolism regulation remains elusive. This study elucidates the specific role of Irisin in mitigating diabetic renal tubular epithelial injury, with a focus on its regulatory mechanisms under glucotoxic conditions. Utilizing streptozotocin (STZ)-induced type 1 diabetes (T1D) mouse models and high glucose (HG)-stimulated HK-2 cells, we demonstrated that STZ-induced DN mice exhibited renal dysfunction, oxidative stress, and iron accumulation. Sustained HG exposure downregulated glutathione peroxidase 4 (GPX4) and xCT while upregulating Ptgs2 and FPN1, indicative of Ferroptosis initiation. Irisin treatment significantly attenuated these pathological changes and ameliorated renal tubular epithelial injury. Mechanistically, this protective effect was mediated through the activation of high-mobility group box-1 (HMGB1), a damage-associated regulator, as observed in both in vivo and in vitro studies. Furthermore, we identified the nuclear translocation of Nrf2 and its downstream target GPX4 in vitro. Specific interference with Nrf2, through both knockdown and overexpression experiments under HG conditions, further demonstrated Irisin's regulatory role on HMGB1. This was validated by assessing tubular epithelial cell viability, alongside cellular levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and Fe
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.