ArticleCell biochemistry and biophysics2024
Quercetin Attenuates Acute Kidney Injury Caused by Cisplatin by Inhibiting Ferroptosis and Cuproptosis.
Article in Cell biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Cuproptosis: New Perspectives for Prevention and Treatment of Osteoarthritis with Chinese Medicine Extracts.Chinese journal of integrative medicine · 2026Review
- Targeting GLS and LPIN2 in renal fibroblasts: potential therapeutic targets for kidney stone disease identified by integrated multi-omics analysis.Urolithiasis · 2026Article
- Copper Metabolism-Related Cell Death in Kidney Diseases: Molecular Mechanisms, Disease-Specific Evidence, and Translational Implications.International journal of molecular sciences · 2026Review
- Copper homeostasis and cuproptosis: molecular mechanisms and therapeutic opportunities.Molecular biomedicine · 2026Review
- Natural compounds targeting inflammatory signaling and cell adhesion molecules in ischemic acute kidney injury.Archives of pharmacal research · 2026Review
- Copper-Induced Nephropathy: Clinical Characterization of 36 Cases and Comprehensive Literature Review.Biological trace element research · 2026Review
- Natural Products in Cancer Prevention and Therapy: Current Challenges and Future Directions.MedComm · 2026Review
- Icariin protects against cisplatin-induced renal injury and ferroptosis via JNK pathway in mice.BMC nephrology · 2026Article
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- Cross-talk among novel programmed cell death pathways: a decisive network in renal ischemia-reperfusion injury.Frontiers in immunology · 2026Review
- Research progress of cuproptosis, ferroptosis, apoptosis, and autophagy in knee osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Yiqi-Wenyang-Tiaoshen Decoction Reduces Cisplatin-Induced Acute Kidney Injury in Rats Through Autophagy and Apoptosis Signaling Pathways Based on Network Pharmacology and Experimental Validation.Mediators of inflammation · 2026Article
- Nephroprotective Effects of Quercetin-Selenium Nanoparticles Against Glycerol-Induced AKI.International journal of molecular sciences · 2025Article
- HMGB1/NF-κB Axis, IL-8, and Cuproptosis Contribute to Cisplatin-Induced Testicular Injury: Protective Potential Effect of Thymol.Biomolecules · 2025Article
- Epigenetic modification of cuproptosis by non-coding RNAs in cancer drug resistance.Molecular cancer · 2025Review
- Cellular senescence in kidney diseases.Chinese medical journal · 2025Review
- Functional, Structural and Genetic Modulation in Plasma and Renal Antioxidant Systems by Quercetin, Catechin and Genistein in Cisplatin-Induced Acute Nephrotoxicity in Wistar Rats.Food science & nutrition · 2025Article
- Association between copper exposure and renal fibrosis in patients with chronic kidney disease: evidence from Mendelian randomization and a retrospective study.Frontiers in public health · 2025Article
- Copper-Induced Cell Death in Renal Diseases: Molecular Mechanisms and Therapeutic Implications.Drug design, development and therapy · 2025Review
- Synergistic chemotherapy and immunomodulatory effects of Quercetin in cancer: a review.Frontiers in immunology · 2025Review
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Authors and funding
3 authors.
Funding
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Abstract
Ferroptosis, an iron- and ROS-dependent form of regulated cell death. Cuproptosis is a novel form of cellular demise mode. Quercetin, a natural flavonoid, has demonstrated a range of pharmacological activities, including anti-cancer, anti-inflammatory, and antioxidant properties. In this research, we investigated the quercetin effect on cisplatin-induced acute kidney and its mechanism associated ferroptosis and cuproptosis. The HK-2 cells were used in this research. Cell viability was evaluated using the CCK-8 assay. Acute kidney injury (AKI) models were established to perform in vivo experiments. Renal tissue homogenate was used to determine ROS, LPO, MDA, PA, etc., to assess ferroptosis and cuproptosis. To perform bioinformatic analysis, microarray data from the GEO database was utilized. Real-time PCR analysis and ELISA was explored the mechanism of ferroptosis and cuproptosis. We found that ferroptosis and cuproptosis in AKI were abnormally activated caused by cisplatin, and that quercetin attenuated AKI by inhibiting ferroptosis and cuproptosis. QCT suppressed ferroptosis by reducing malondialdehyde (MDA) and ROS levels and increasing glutathione (GSH) levels and alleviated cuproptosis by reducing copper ion, pyruvate (PA) and HSP70 levels. Moreover, bioinformatic analysis revealed that the ferroptosis-related gene SLC7A11 and the cuproptosis-related genes ATP7B and GLS were the differential expression genes. And QCT significantly increased the expression or activity of SLC7A11, GPX4, ATP7B, and GLS in Cis-AKI mice. Our findings highlight the clinical importance of quercetin, which guards against cisplatin-induced acute kidney injury by suppressing ferroptosis and cuproptosis.
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