ArticleAntioxidants (Basel, Switzerland)2025
Mechanisms of Cisplatin-Induced Acute Kidney Injury: The Role of NRF2 in Mitochondrial Dysfunction and Metabolic Reprogramming.
Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The trial behind it
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Who cites it
19 citing papers in PubMed.
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Ameliorative effect of rufigallol on cisplatin-induced nephrotoxicity in rats: biochemical and histopathological evaluation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Rutin-Functionalized Selenium Nanoparticles Attenuate Cisplatin-Induced Cardiohepatic Injury in Rats: Modulation of ER Stress-Related Gene Expression and Mitochondrial Apoptotic Markers.International journal of molecular sciences · 2026Article
- Sulforaphane attenuates cisplatin‑induced acute kidney injury by inhibiting oxidative stress, inflammation and apoptosis via regulation of NRF2.Molecular medicine reports · 2026Article
- Proanthocyanidins Attenuate Cisplatin-Induced Acute Kidney Injury and are Associated With Reshaping Gut Microbiota and Restoring Redox Homeostasis.Molecular nutrition & food research · 2026Article
- Renoprotective effects of perampanel against cisplatin-induced acute kidney injury: managing NLRP3-pyroptosis and enhancement of antioxidant defense.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Carob pod aqueous extract potentiates cisplatin efficacy and reduces toxicity in experimental hepatocellular carcinoma via mitochondrial and inflammatory pathway modulation.Bioresources and bioprocessing · 2026Article
- Magnesium as a Bioenergetic Checkpoint Linking Mitochondrial Function, Metabolic Disease, and Aging.Aging cell · 2026Review
- Dapagliflozin attenuates cisplatin-induced nephrotoxicity in rats through modulation of ROS/NF-κB, BCL2/Bax and PINK1/Parkin signaling pathways.Scientific reports · 2026Article
- Alpha-1 Antitrypsin Protects Against Cisplatin-Induced Acute Kidney Injury by Restoring Redox and Mitochondrial Homeostasis.Biomolecules · 2026Article
- Review
- Article
- Loss of KLF15 expression characterizes proximal tubule injury in cisplatin-induced acute kidney injury: A multi-omics study.Current research in toxicology · 2026Article
- Poor prognosis of acute kidney injury superimposed on chronic kidney disease: potential mechanisms, risk factors and novel biomarkers.Frontiers in molecular biosciences · 2026Review
- Mitochondrial calcium uniporter-mediated mitochondrial dynamics imbalance contributes to contrast medium-induced renal tubular cell injury.Frontiers in molecular biosciences · 2026Article
- Formononetin alleviated cisplatin-induced acute kidney injury by orchestrating renal tubular cell ferroptosis via PI3K/AKT/NRF2 pathway.Frontiers in pharmacology · 2026Article
- Article
- Pervasive food contaminant ochratoxin-A induces energy crisis: Mitochondrial dysfunction in human primary proximal tubule cells.Toxicology reports · 2025Article
- Leukocyte Ratios Predict Metastasis, Recurrence, and Mortality in Breast Cancer Patients Receiving Cytotoxic Chemotherapy.Medical sciences (Basel, Switzerland) · 2025Observational
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Cisplatin (Cis) is a widely used chemotherapy drug, but its nephrotoxicity limits its clinical application. Acute kidney injury (AKI) is a common complication, restricting long-term use. This study investigates the mechanisms of cisplatin-induced AKI and explores potential therapeutic targets. C57BL/6J mice were intraperitoneally injected with 20 mg/kg cisplatin to establish an AKI model. Serum creatinine, urea nitrogen, and tubular injury biomarkers (NGAL, KIM-1) progressively increased, indicating kidney dysfunction. Mitochondrial ATP levels significantly decreased, along with reduced mitochondrial fission and fusion, suggesting mitochondrial dysfunction. Increased oxidases and reduced antioxidants indicated redox imbalance, and metabolic reprogramming was observed, with lipid deposition, impaired fatty acid oxidation (FAO), and enhanced glycolysis in proximal tubular epithelial cells (PTECs). Nuclear factor erythroid 2-related factor 2 (NRF2) is a key transcriptional regulator of redox homeostasis and mitochondrial function. We found NRF2 levels increased early in AKI, followed by a decrease in vivo and in vitro, suggesting activation in the stress response.
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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 Socratic graph.