ArticleRedox biology2022
Farnesoid X receptor protects against cisplatin-induced acute kidney injury by regulating the transcription of ferroptosis-related genes.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- Ferroptosis inhibition as a renoprotective strategy in cisplatin-induced acute kidney injury: multilevel meta-analysis of mechanistic biomarkers.Frontiers in medicine · 2026Pooled it
- Exploring therapeutic mechanisms of Chuan Huang Fang-II in the treatment of acute kidney injury on chronic kidney disease patients from the perspective of lipidomics.Renal failure · 2024Trial
- Mitophagy in cisplatin-induced kidney injury: regulatory mechanisms and therapeutic targets.Annals of medicine · 2026Review
- Rosmarinic Acid Alleviates Cisplatin-Induced Acute Kidney Injury by Targeting FYN to Regulate Ferroptosis.Food science & nutrition · 2026Article
- Kidney-Targeted Cilastatin Nanoparticles Inhibit DPEP1-Mediated Ferroptosis for Acute Kidney Injury Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PLA2G2F suppresses ferroptosis through phospholipid remodeling.Nature structural & molecular biology · 2026Article
- The nuclear receptor ESRRA is a crucial regulator of acute kidney injury through inhibition of the lipophagy-ferroptosis axis.Autophagy · 2026Article
- Article
- Impaired fatty acid metabolism in AKI: experimental evidence - a narrative review.BMC nephrology · 2026Review
- Concurrent Evaluation of Liver and Kidney Function by NIR-IIChemical & biomedical imaging · 2026Article
- Mechanisms and reversal strategies of liver fibrosis: from regulation of cell fate to clinical translation.Journal of translational medicine · 2026Review
- Gut microbiota-induced perturbation in bile acids alter keratinocyte lipid metabolism via FXR-NQO1 signaling in psoriasis.Nature communications · 2026Article
- HucMSC-derived exosomes alleviate inflammatory bowel disease via upregulating FXR to suppress macrophage ferroptosis.Biology direct · 2026Article
- Sialic acid exacerbates polycystic ovary syndrome in mice by modulating gut microbiota-mediated bile acid metabolism and FXR activation.Nature communications · 2026Article
- Angiotensin II-Induced Ferroptosis in Epithelial Cells Contributes to Kidney Injury via SP1-DPEP1-Mediated SLC3A2 Degradation.Diabetes · 2026Article
- ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Phenothiazine alleviates cisplatin-mediated acute kidney injury by inhibiting ferroptosis.Cell and tissue research · 2026Article
- GUDCA drives colorectal cancer progression via ALKBH5-mediated m6A modification of ENO1 and glycolytic reprogramming.Frontiers in pharmacology · 2026Article
- Ferroptosis: A Double-Edged Sword in Cisplatin-Based Cancer Therapy and Acute Kidney Injury.Cancer management and research · 2026Review
- Targeting the NSUN2-DHODH axis reverses ferroptosis resistance and oxaliplatin resistance in colorectal cancer.Frontiers in pharmacology · 2026Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The side effects of cisplatin, a widely used chemotherapeutic agent, include nephrotoxicity. Previous studies have reported that cisplatin induces ferroptosis and lipid peroxide accumulation. Ferroptosis, a type of regulated cell death, is characterized by iron-dependent lipid peroxidation. Although previous studies have examined the regulation of ferroptosis in acute kidney injury (AKI), the regulatory mechanism of ferroptosis has not been elucidated. Here, the ability of activated farnesoid X receptor (FXR) to attenuate cisplatin-induced AKI through the regulation of ferroptosis was examined. FXR deficiency exhibited more ferroptosis responses, such as increase in lipid peroxidation, iron content and heme oxygenase 1 protein, and a decrease in glutathione/glutathione disulfide ratio and glutathione peroxidase 4 levels in HK2 cells and mice. Increased blood urea nitrogen, serum creatinine, and ferroptotic responses in the cisplatin-induced AKI mouse model were mitigated upon treatment with the FXR agonist GW4064 but were exacerbated in FXR knockout mice. RNA sequencing analysis revealed that ferroptosis-associated genes were novel targets of FXR. FXR agonist upregulated the expression of lipid and glutathione metabolism-related genes and downregulated cell death-related genes. Additionally, chromatin immunoprecipitation assays, using mice renal tissues, revealed that agonist-activated FXR could bind to its known target genes (Slc51a, Slc51b, Osgin1, and Mafg) and ferroptosis-related genes (Aifm2, Ggt6, and Gsta4). Furthermore, activated FXR-dependent MAFG, a transcriptional repressor, could bind to Hmox1, Nqo1, and Tf in the renal tissues of FXR agonist-treated mice. These findings indicate that activated FXR regulates the transcription of ferroptosis-related genes and protects against cisplatin-induced AKI.
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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.