ArticleThe Journal of biological chemistry2011
Vav family Rho guanine nucleotide exchange factors regulate CD36-mediated macrophage foam cell formation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Research Progress on the ARHGEF Family in Cardiovascular Diseases.Cell biochemistry and function · 2026Review
- Vav family exchange factors: Potential regulator in atherosclerosis.Biochemistry and biophysics reports · 2024Review
- CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway.Journal of neuroinflammation · 2024Article
- TheJournal of inflammation research · 2023Article
- Endothelial cell-specific deletion of a microRNA accelerates atherosclerosis.Atherosclerosis · 2022Article
- Identification and functional analysis of a biflavone as a novel inhibitor of transient receptor potential vanilloid 4-dependent atherogenic processes.Scientific reports · 2021Article
- The neurorepellent, Slit2, prevents macrophage lipid loading by inhibiting CD36-dependent binding and internalization of oxidized low-density lipoprotein.Scientific reports · 2021Article
- Siglec-E retards atherosclerosis by inhibiting CD36-mediated foam cell formation.Journal of biomedical science · 2021Article
- The Emerging Role of Rho Guanine Nucleotide Exchange Factors in Cardiovascular Disorders: Insights Into Atherosclerosis: A Mini Review.Frontiers in cardiovascular medicine · 2021Review
- Endothelial Cell CD36 Reduces Atherosclerosis and Controls Systemic Metabolism.Frontiers in cardiovascular medicine · 2021Article
- CD36 facilitates fatty acid uptake by dynamic palmitoylation-regulated endocytosis.Nature communications · 2020Article
- Role of macrophage TRPV4 in inflammation.Laboratory investigation; a journal of technical methods and pathology · 2020Review
- The three members of the Vav family proteins form complexes that concur to foam cell formation and atherosclerosis.Journal of lipid research · 2019Article
- TRPV4 is a regulator in P. gingivalis lipopolysaccharide-induced exacerbation of macrophage foam cell formation.Physiological reports · 2019Article
- Constitutive and stimulated macropinocytosis in macrophages: roles in immunity and in the pathogenesis of atherosclerosis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Article
- ROS via BTK-p300-STAT1-PPARγ signaling activation mediates cholesterol crystals-induced CD36 expression and foam cell formation.Redox biology · 2017Article
- Identification of novel genes and pathways in carotid atheroma using integrated bioinformatic methods.Scientific reports · 2016Article
- Spiromastixones Inhibit Foam Cell Formation via Regulation of Cholesterol Efflux and Uptake in RAW264.7 Macrophages.Marine drugs · 2015Article
- Oxidized LDL-bound CD36 recruits an Na⁺/K⁺-ATPase-Lyn complex in macrophages that promotes atherosclerosis.Science signaling · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Lipid-laden macrophages or "foam cells" are the primary components of the fatty streak, the earliest atherosclerotic lesion. Although Vav family guanine nucleotide exchange factors impact processes highly relevant to atherogenesis and are involved in pathways common to scavenger receptor CD36 signaling, their role in CD36-dependent macrophage foam cell formation remains unknown. The goal of the present study was to determine the contribution of Vav proteins to CD36-dependent foam cell formation and to identify the mechanisms by which Vavs participate in the process. We found that CD36 contributes to activation of Vav-1, -2, and -3 in aortae from hyperlipidemic mice and that oxidatively modified LDL (oxLDL) induces activation of macrophage Vav in vitro in a CD36 and Src family kinase-dependent manner. CD36-dependent uptake of oxLDL in vitro and foam cell formation in vitro and in vivo was significantly reduced in Vav null macrophages. These studies for the first time link CD36 and Vavs in a signaling pathway required for macrophage foam cell formation.
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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.