ArticleJournal of applied toxicology : JAT2026
L-Carnitine Attenuates Methotrexate-Induced Nephrotoxicity by Modulating BAX/BCL2 Apoptotic Signaling and Preserving Podocyte, Endothelial, and Tubular Integrity.
Article in Journal of applied toxicology : JAT, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- L-Carnitine Attenuates Methotrexate-Induced Nephrotoxicity by Modulating BAX/BCL2 Apoptotic Signaling and Preserving Podocyte, Endothelial, and Tubular Integrity.Journal of applied toxicology : JAT · 2026Article
- Dexpanthenol Attenuates Methotrexate-Induced Nephrotoxicity Through Modulation of NF-κB-Mediated Inflammation and SIRT1/PGC-1α-NRF2/HO-1-Associated Oxidative Stress Pathways.Journal of biochemical and molecular toxicology · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Methotrexate (MTX), a common chemotherapeutic and immunosuppressive drug, is limited by dose-dependent nephrotoxicity mediated by oxidative stress, mitochondrial dysfunction, and apoptosis. L-carnitine (LCR), a mitochondrial cofactor with antioxidant and anti-apoptotic properties, may counteract these mechanisms. This study aims to determine whether LCR mitigates MTX-induced nephrotoxicity by rebalancing the BAX/BCL2 apoptotic axis and preserving renal compartment integrity (endothelial CD31, tubular cytokeratin, podocyte WT1). Twenty-four female Wistar rats were randomized into Control, MTX (20 mg/kg, i.p., Day 5), LCR (200 mg/kg/day, i.p., 10 days), and MTX + LCR groups (n = 6 each). Renal injury was assessed by serum creatinine, urea, BUN, histopathology, immunohistochemistry (CD31, cytokeratin, WT1), and RT-qPCR for BAX/BCL2. MTX impaired renal function, caused vascular hyperemia, hemorrhage, and tubular necrosis, increased CD31, cytokeratin, and BAX and decreased WT1 and BCL2. LCR co-treatment improved biochemical indices, reduced lesions, decreased CD31 and cytokeratin, partially restored WT1 and re-balanced apoptosis (BAX↓, BCL2↑). LCR disrupts oxidative stress, the mitochondrial apoptosis cascade, and preserves endothelial, tubular, and podocyte integrity in MTX nephrotoxicity.
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Registered trials
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