ArticleThe Journal of clinical investigation2010
CD36 participates in a signaling pathway that regulates ROS formation in murine VSMCs.
Article in The Journal of clinical investigation, 2010. 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.
What it found
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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
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- The role of CD36 in immune function: bridging innate and adaptive responses.Frontiers in immunology · 2026Pooled it
- A Common CD36 Variant Influences Endothelial Function and Response to Treatment with Phosphodiesterase 5 Inhibition.The Journal of clinical endocrinology and metabolism · 2016Trial
- Treml4 Drives Microglial Activation via the Lyn/Syk/ERK Pathway in Sepsis-Associated Encephalopathy.Neurochemical research · 2026Article
- TM4SF5-mediated KEAP1 Regulation in Hepatocytes Irrelevant to NRF2 Expression and Activity Promotes Oxidative Stress and Inflammation to Develop Metabolic Dysfunction-Associated Steatotic Liver Disease.International journal of biological sciences · 2026Article
- The immune receptor FcRγ-chain mediates CD36-induced platelet activation and thrombosis by oxidized low-density lipoproteins.Blood advances · 2025Article
- Thirty years of NRF2: advances and therapeutic challenges.Nature reviews. Drug discovery · 2025Review
- Targeting cholesterol-driven pyroptosis: a promising strategy for the prevention and treatment of atherosclerosis.Molecular biology reports · 2025Review
- Deciphering the Role of CD36 in Gestational Diabetes Mellitus: Linking Fatty Acid Metabolism and Inflammation in Disease Pathogenesis.Journal of inflammation research · 2025Review
- Article
- Mutant p53 protects triple-negative breast adenocarcinomas from ferroptosis in vivo.Science advances · 2024Article
- Targeting Cysteine Oxidation in Thrombotic Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- Thymidine Phosphorylase Promotes Abdominal Aortic Aneurysm via VSMC Modulation and Matrix Remodeling in Mice and Humans.Cardiovascular therapeutics · 2024Article
- Chlorogenic Acid Alleviates LPS-Induced Inflammation and Oxidative Stress by Modulating CD36/AMPK/PGC-1α in RAW264.7 Macrophages.International journal of molecular sciences · 2023Article
- Extract ofAntioxidants (Basel, Switzerland) · 2023Article
- PARP2 poly(ADP-ribosyl)ates nuclear factor erythroid 2-related factor 2 (NRF2) affecting NRF2 subcellular localization.Scientific reports · 2023Article
- A CD36 transmembrane domain peptide interrupts CD36 interactions with membrane partners on macrophages and inhibits atherogenic functions.Translational research : the journal of laboratory and clinical medicine · 2023Article
- CD36, a signaling receptor and fatty acid transporter that regulates immune cell metabolism and fate.The Journal of experimental medicine · 2022Review
- Article
- Review
- Niclosamide downregulates LOX-1 expression in mouse vascular smooth muscle cells and changes the composition of atherosclerotic plaques in ApoEHeart and vessels · 2022Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 6 institutions in 3 countries.
Funding
Abstract
CD36 is a membrane glycoprotein expressed on platelets, monocytes, macrophages, and several other cell types that was recently demonstrated to be involved in platelet activation in response to oxidized phospholipids, including oxidized LDL. Although the role of CD36 in other vascular cells has not been well defined, previous studies have demonstrated that cd36-knockout (cd36-/-) mice have prolonged thrombosis times after vascular injury, which can be protective in the state of hyperlipidemia. Here, we found significantly less ROS in the vessel walls of cd36-/- mice compared with WT after chemically induced arterial injury, suggesting that CD36 may contribute to ROS generation in the VSMCs themselves. Gene expression analysis revealed that the antioxidant enzymes peroxiredoxin-2 (Prdx2) and heme oxygenase-1 were upregulated in cd36-/- VSMCs. Molecular dissection of the pathway in isolated mouse VSMCs revealed CD36 ligand-dependent induction of Fyn phosphorylation, with subsequent phosphorylation and degradation of the redox-sensitive transcription factor Nrf2. Chromatin immunoprecipitation experiments further showed that Nrf2 directly occupied the Prdx2 promoter. The importance of this pathway was evidenced by increased ROS generation in prdx2-/- mice and decreased thrombosis times in both prdx2-/- and nrf2-/- mice after vascular injury. These data suggest that CD36-mediated downregulation of antioxidant systems in VSMCs may contribute to its prothrombotic, proinflammatory, and atherogenic effects.
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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.