ArticleGenes & diseases2024
CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury.
Article in Genes & diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Study of CD36 receptor gene expression in obese and non-obese chronic kidney disease patients.Molecular biology reports · 2026Article
- Research Progress on the Treatment of Renal Injury with Esculetin: Multi-Target Pharmacological Mechanism and Clinical Translation Prospect.International journal of molecular sciences · 2026Review
- CD36 enhances sensitivity of triple negative breast cancer cells to palmitate-induced ferroptosis.Cell death & disease · 2026Article
- Ferroptosis suppressor protein 1-mediated ferroptosis suppression in sepsis: non-canonical antioxidant pathways, inflammatory regulation, and therapeutic perspectives.Frontiers in immunology · 2026Review
- Mesenchymal stem cell-derived extracellular vesicles for disease therapy by regulating ferroptosis: focus on diabetes mellitus and diabetic complications.Stem cell research & therapy · 2025Review
- Single-Cell Transcriptomics Unravels Growth Factor Erv1-Like Mediated Ferroptosis as a Key Driver of Intestinal Epithelial Dysfunction in Ulcerative Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The impact of lipid metabolism on ferroptosis in myocardial ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2025Review
- The role of ferroptosis in acute kidney injury: the preemptive mode of cell death and the bridging effect.Renal failure · 2025Review
- The Role of Ubiquitination and Deubiquitination in the Pathogenesis of Acute Kidney Injury: Progress in Research.Biomedicines · 2025Review
- CDC26 facilitates ferroptosis through SLC7A11 degradation and cell cycle arrest.Clinical and experimental medicine · 2025Article
- Tirzepatide, a dual GIP/GLP-1 receptor agonist, alleviates metabolic dysfunction-associated steatotic liver disease by reducing the expression of CD36 and OBP2A.Genes & diseases · 2025Article
- Acute kidney injury: pathogenesis and therapeutic interventions.Molecular biomedicine · 2025Review
- Ferroptosis in Cancer and Inflammatory Diseases: Mechanisms and Therapeutic Implications.MedComm · 2025Review
- Mechanisms of Cisplatin-Induced Acute Kidney Injury: The Role of NRF2 in Mitochondrial Dysfunction and Metabolic Reprogramming.Antioxidants (Basel, Switzerland) · 2025Article
- SLC25A1 and ACLY maintain cytosolic acetyl-CoA and regulate ferroptosis susceptibility via FSP1 acetylation.The EMBO journal · 2025Article
- The role of ferroptosis in acute kidney injury: mechanisms and potential therapeutic targets.Molecular and cellular biochemistry · 2025Review
- Alliin mitigates the acute kidney injury by suppressing ferroptosis via regulating the Nrf2/GPX4 axis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Exploring Liraglutide's mechanism in reducing renal fibrosis: the Fsp1-CoQ10-NAD(P)H pathway.Scientific reports · 2025Article
- Mechanism of Ferroptosis and Its Role in Disease Development.International journal of biological sciences · 2025Review
- Transformation of acute kidney injury to chronic kidney disease: the interaction between mitophagy and NLRP3 inflammasome.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxidative species (ROS) production-driven ferroptosis plays a role in acute kidney injury (AKI). However, its exact molecular mechanism is poorly understood. Scavenger receptor CD36 has important roles in oxidizing lipids, lipid accumulation, metabolic syndrome, and insulin resistance in chronic kidney disease, but its roles remain unexplored in AKI. The present study investigated the role and mechanism of CD36 in regulating proximal tubular cell ferroptosis and AKI. The expression of CD36 was found to be significantly up-regulated in AKI renal tissues and correlated with renal function, which might serve as an independent biomarker for AKI patients. Moreover, in adult mice subjected to AKI, deletion of CD36 (CD36
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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 OpenQuestion graph.