ArticleThe Journal of biological chemistry2011
CD36 protein is involved in store-operated calcium flux, phospholipase A2 activation, and production of prostaglandin E2.
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 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 89 citations in OpenAlex.
- The Dark Triad of Particulate Matter, Oxidative Stress and Coronary Artery Disease: What About the Antioxidant Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Dietary Oleic Acid and SCD16 and ELOVL6 Estimated Activities Can Modify Erythrocyte Membrane n-3 and n-6 HUFA Partition: A Pilot Study.Current issues in molecular biology · 2025Article
- Diabetes mellitus-driven pulmonary injury: multidimensional mechanisms linking metabolic dysregulation to gut-lung axis and promising therapies.Frontiers in pharmacology · 2025Review
- The endothelium: gatekeeper to lung ischemia-reperfusion injury.Respiratory research · 2024Review
- Article
- LncGenes · 2023Article
- Role of adipose tissue macrophages in obesity-related disorders.The Journal of experimental medicine · 2022Article
- Modulation of endothelium function by fatty acids.Molecular and cellular biochemistry · 2022Review
- Cardiac immune cell infiltration associates with abnormal lipid metabolism.Frontiers in cardiovascular medicine · 2022Article
- Lipid metabolism in ferroptosis and ferroptosis-based cancer therapy.Frontiers in oncology · 2022Review
- The computational analyses, molecular dynamics of fatty-acid transport mechanism to the CD36 receptor.Scientific reports · 2021Article
- The Kidney-Related Effects of Polystyrene Microplastics on Human Kidney Proximal Tubular Epithelial Cells HK-2 and Male C57BL/6 Mice.Environmental health perspectives · 2021Article
- Lipid Metabolism and Ferroptosis.Biology · 2021Review
- Endothelial Cell Receptors in Tissue Lipid Uptake and Metabolism.Circulation research · 2021Review
- Indomethacin Treatment Post-irradiation Improves Mouse Parotid Salivary Gland Function via Modulation of Prostaglandin EFrontiers in bioengineering and biotechnology · 2021Article
- Article
- Calcium regulation of T cell metabolismCurrent opinion in physiology · 2020Article
- Novel role of the ER/SR CaAmerican journal of physiology. Heart and circulatory physiology · 2019Article
- Distinct metabolic patterns during microglial remodeling by oleate and palmitate.Bioscience reports · 2019Article
- On the Mechanisms of Action of the Low Molecular Weight Fraction of Commercial Human Serum Albumin in Osteoarthritis.Current rheumatology reviews · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The scavenger receptor FAT/CD36 contributes to the inflammation associated with diabetes, atherosclerosis, thrombosis, and Alzheimer disease. Underlying mechanisms include CD36 promotion of oxidative stress and its signaling to stress kinases. Here we document an additional mechanism for the role of CD36 in inflammation. CD36 regulates membrane calcium influx in response to endoplasmic reticulum (ER) stress, release of arachidonic acid (AA) from cellular membranes by cytoplasmic phospholipase A(2)α (cPLA(2)α) and contributes to the generation of proinflammatory eicosanoids. CHO cells stably expressing human CD36 released severalfold more AA and prostaglandin E(2) (PGE(2)), a major product of AA metabolism by cyclooxygenases, in response to thapsigargin-induced ER stress as compared with control cells. Calcium influx after ER calcium release resulted in phosphorylation of cPLA(2) and its translocation to membranes in a CD36-dependent manner. Peritoneal macrophages from CD36(-/-) mice exhibited diminished calcium transients and reduced AA release after thapsigargin or UTP treatment with decreased ERK1/2 and cPLA(2) phosphorylation. However, PGE(2) production was unexpectedly enhanced in CD36(-/-) macrophages, which probably resulted from a large induction of cyclooxygenase 2 mRNA and protein. The data demonstrate participation of CD36 in membrane calcium influx in response to ER stress or purinergic receptor stimulation resulting in AA liberation for PGE(2) formation. Collectively, these results identify a mechanism contributing to the pleiotropic proinflammatory effects of CD36 and suggest that its targeted inhibition may reduce the acute inflammatory response.
Indexed as
Identifiers
What OpenQuestion holds
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.