ArticleScience signaling2015
Oxidized LDL-bound CD36 recruits an Na⁺/K⁺-ATPase-Lyn complex in macrophages that promotes atherosclerosis.
Article in Science signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 60 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
60 citing papers in PubMed, 92 citations in OpenAlex.
- Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Multi-omics characterization of anoikis-related hub genes and macrophage-centered immune persistence with validation of HAVCR2 in atherosclerosis.Frontiers in immunology · 2026Article
- FcR γ-chain and platelet hyperactivity.Blood advances · 2025Article
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.bioRxiv : the preprint server for biology · 2025Article
- Investigation of CD36 interactome provides insights into multimolecular complexes necessary for anti-angiogenic signalling.bioRxiv : the preprint server for biology · 2025Article
- Article
- Oxidized LDL stimulates PKM2-mediated mtROS production and phagocytosis.Journal of lipid research · 2025Article
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- Dissecting Causal Relationship Among Immune Cells, Plasma Metabolites and Coronary Atherosclerosis: A Mendelian Randomization Study.ImmunoTargets and therapy · 2025Article
- Unveiling ammonia-induced cell death: a new frontier in clear cell renal cell carcinoma prognosis.Frontiers in immunology · 2025Article
- Macadamia (Foods (Basel, Switzerland) · 2024Article
- Targeting mitochondrial dynamics and redox regulation in cardiovascular diseases.Trends in pharmacological sciences · 2024Review
- Targeting Cysteine Oxidation in Thrombotic Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- Troponin I Tyrosine Phosphorylation Beneficially Accelerates Diastolic Function.Circulation research · 2024Article
- CD36 restricts lipid-associated macrophages accumulation in white adipose tissues during atherogenesis.Frontiers in cardiovascular medicine · 2024Article
- CD36/Lyn kinase interactions within macrophages promotes pulmonary fibrosis in response to oxidized phospholipid.Respiratory research · 2023Article
- Nuclear FAK in endothelium: An intrinsic inhibitor of NF-κB activation in atherosclerosis.Atherosclerosis · 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
- Contribution of adipocyte Na/K-ATPase α1/CD36 signaling induced exosome secretion in response to oxidized LDL.Frontiers in cardiovascular medicine · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
One characteristic of atherosclerosis is the accumulation of lipid-laden macrophage foam cells in the arterial wall. We have previously shown that the binding of oxidized low-density lipoprotein (oxLDL) to the scavenger receptor CD36 activates the kinase Lyn, initiating a cascade that inhibits macrophage migration and is necessary for foam cell generation. We identified the plasma membrane ion transporter Na(+)/K(+)-ATPase as a key component in the macrophage oxLDL-CD36 signaling axis. Using peritoneal macrophages isolated from Atp1a1 heterozygous or Cd36-null mice, we demonstrated that CD36 recruited an Na(+)/K(+)-ATPase-Lyn complex for Lyn activation in response to oxLDL. Macrophages deficient in the α1 Na(+)/K(+)-ATPase catalytic subunit did not respond to activation of CD36, showing attenuated oxLDL uptake and foam cell formation, and oxLDL failed to inhibit migration of these macrophages. Furthermore, Apoe-null mice, which are a model of atherosclerosis, were protected from diet-induced atherosclerosis by global deletion of a single allele encoding the α1 Na(+)/K(+)-ATPase subunit or reconstitution with macrophages that lacked an allele encoding the α1 Na(+)/K(+)-ATPase subunit. These findings identify Na(+)/K(+)-ATPase as a potential target for preventing or treating atherosclerosis.
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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.