ArticleOral diseases2017
CD36 is upregulated in mice with periodontitis and metabolic syndrome and involved in macrophage gene upregulation by palmitate.
Article in Oral diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Host insulin resistance caused byFrontiers in cellular and infection microbiology · 2023Pooled it
- CD36 Gene Polymorphisms Are Associated with Intracerebral Hemorrhage Susceptibility in a Han Chinese Population.BioMed research international · 2017Trial
- The Role of Oral Pathobionts' Outer Membrane Vesicles in Cancer Pathology and Therapeutic Development.Cells · 2026Review
- Impaired Mitophagy-Induced Apoptosis of Gingival Fibroblasts Exacerbates Diabetic Periodontitis Via THBS-1/CD36-Dependent Macrophage Activation.Inflammation · 2026Article
- Dietary lipids induce PPARd and BCL6 to repress macrophage IL-23 induction after intestinal injury and LPS exposure.Scientific reports · 2025Article
- Unraveling the Complex Nexus of Macrophage Metabolism, Periodontitis, and Associated Comorbidities.Journal of innate immunity · 2025Review
- GPR40/GPR120 Agonist GW9508 Improves Metabolic Syndrome-Exacerbated Periodontitis in Mice.International journal of molecular sciences · 2024Article
- Palmitate Stimulates Expression of the von Willebrand Factor and Modulates Toll-like Receptors Level and Activity in Human Umbilical Vein Endothelial Cells (HUVECs).International journal of molecular sciences · 2023Article
- Association between metabolic syndrome components and gingival bleeding is women-specific: a nested cross-sectional study.Journal of translational medicine · 2023Article
- Periodontal treatment and microbiome-targeted therapy in management of periodontitis-related nonalcoholic fatty liver disease with oral and gut dysbiosis.World journal of gastroenterology · 2023Review
- Osteoporosis and Alveolar Bone Health in Periodontitis Niche: A Predisposing Factors-Centered Review.Cells · 2022Review
- Association between metabolic syndrome and periodontitis: The role of lipids, inflammatory cytokines, altered host response, and the microbiome.Periodontology 2000 · 2021Review
- Long Chain Fatty Acids as Modulators of Immune Cells Function: Contribution of FFA1 and FFA4 Receptors.Frontiers in physiology · 2021Review
- Article
- Replacing Saturated Fat With Unsaturated Fat in Western Diet Reduces Foamy Monocytes and Atherosclerosis in MaleArteriosclerosis, thrombosis, and vascular biology · 2020Article
- The effect of palmitic acid on inflammatory response in macrophages: an overview of molecular mechanisms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Review
- Potential Role of Free Fatty Acids in the Pathogenesis of Periodontitis and Primary Sjögren's Syndrome.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWe reported that high-fat diet (HFD)-induced metabolic syndrome (MetS) exacerbates lipopolysaccharide (LPS)-stimulated periodontitis and palmitate, the major saturated fatty acid in the HFD, amplified LPS-stimulated gene expression in vitro. As CD36 is a major receptor for fatty acids, we investigated periodontal CD36 expression in mice with periodontitis and MetS, and the role of CD36 in inflammatory gene expression in macrophages stimulated by palmitate.
methodsMetS and periodontitis were induced in mice by HFD and periodontal injection of LPS, respectively. The periodontal CD36 expression and its relationship with alveolar bone loss were studied using immunohistochemistry, real-time PCR, and correlation analysis. The role of CD36 in upregulation of inflammatory mediators by LPS and palmitate in macrophages was assessed using pharmacological inhibitor and small interfering RNA.
resultsPeriodontal CD36 expression was higher in mice with both MetS and periodontitis than that in mice with periodontitis or MetS alone and was correlated with osteoclastogenesis and alveolar bone loss. In vitro studies showed that CD36 expression in macrophages was upregulated by LPS and palmitate, and targeting CD36 attenuated palmitate-enhanced gene expression.
conclusionCD36 expression is upregulated in mice with periodontitis and MetS and involved in gene expression in macrophages stimulated by palmitate and LPS.
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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.