ArticleToxicology reports2026
Azilsartan as a novel anti-ferriptotic agent via the upregulation of the Nrf2/HO-1/SLC7A11/GPX4 axis and downregulation of inflammatory pathways in folic acid-induced acute kidney injury in male mice.
Article in Toxicology reports, 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.
- Telmisartan protects male reproductive function by modulating biochemical, oxidative stress, apoptosis, and DNA integrity in cyclophosphamide-exposed rats.Toxicology reports · 2026Article
- L-carvone protects against myoglobinuric acute tubular necrosis via inhibition of NF-κB and caspase-dependent apoptotic pathways.Toxicology reports · 2026Article
- Mechanistic insights into nicardipine's anti-colitic action: inhibition of pro-inflammatory cytokines, attenuation of oxidative stress, and protection of the mucosal barrier.Molecular biology reports · 2026Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Purpose: Azilsartan, a unique angiotensin II receptor blocker (ARB) with an oxo-oxadiazole ring, exhibits antioxidant and anti-inflammatory properties, but its role in ferroptosis-mediated AKI remains unexplored. This study investigates whether azilsartan protects against FA-induced AKI in male mice by attenuating ferroptosis, modulating iron metabolism, and suppressing inflammatory signaling. Methods: 42 male C57BL/6 J mice were randomized into six groups: control, FA-induced AKI, three azilsartan doses (1, 3, 5 mg/kg), and ferrostatin-1 (Fer-1) as a positive control. Azilsartan or Fer-1 was administered for 7 days before FA injection (250 mg/kg, i.p.) and continued for 3 days post-induction. Renal function (serum urea, creatinine), ferroptosis markers (GPX4, MDA, Nrf2, SLC7A11, HO-1), iron-handling proteins (ferritin, TfR1), inflammatory mediators (TNF-α, NF-κB p65), and histopathology were assessed. Results: FA-AKI caused marked renal dysfunction, elevated KIM-1, lipid peroxidation, depletion of GPX4, downregulation of Nrf2/HO-1/SLC7A11 and TfR1, reduction of transferrin levels, and inflammatory activation. Azilsartan improved renal function and histology in a dose-dependent manner, restored GPX4, reduced MDA, upregulated Nrf2/HO-1/SLC7A11 and TfR1, increased ferritin levels, and suppressed TNF-α/NF-κB. High-dose azilsartan achieved effects comparable to those of Fer-1. Conclusion: Azilsartan confers potent protection against FA-induced AKI by activating the Nrf2/HO-1/SLC7A11/GPX4 axis, reducing lipid peroxidation, normalizing iron metabolism, and attenuating inflammation. These findings support azilsartan's potential as a repurposed therapy for ferroptosis-driven renal injury.
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