ArticlePloS one2015
CD36/SR-B2-TLR2 Dependent Pathways Enhance Porphyromonas gingivalis Mediated Atherosclerosis in the Ldlr KO Mouse Model.
Article in PloS one, 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 31 papers.
What it found
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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.
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
31 citing papers in PubMed, 52 citations in OpenAlex.
- Periodontal disease and cardiovascular events: mechanisms, biomarkers, and clinical translation.NPJ cardiovascular health · 2026Review
- From gum inflammation to oral cancers: pyroptosis as the molecular torchbearer in periodontitis-driven carcinogenesis.Discover oncology · 2025Review
- Unveiling the Molecular Crosstalk Between Periodontal and Cardiovascular Diseases: A Systematic Review.Dentistry journal · 2025Review
- Macrophage pyroptosis in atherosclerosis: therapeutic potential.Acta biochimica et biophysica Sinica · 2025Review
- Regulation of pyroptosis by natural products in atherosclerosis: mechanisms and therapeutic potential.Frontiers in pharmacology · 2025Review
- PPARα modulation of macrophage polarization and inflammatory signaling in mimic periodontitis.Journal of applied oral science : revista FOB · 2025Article
- Integrative analysis of gene and protein expression in atherosclerosis-related pathways modulated by periodontal pathogens. Systematic review.The Japanese dental science review · 2023Review
- Loricrin and Cytokeratin Disorganisation in Severe Forms of Periodontitis.International dental journal · 2023Article
- Intracranial Aneurysms and Lipid Metabolism Disorders: From Molecular Mechanisms to Clinical Implications.Biomolecules · 2023Review
- RhoA/ROCK1 regulates the mitochondrial dysfunction through Drp1 induced by Porphyromonas gingivalis in endothelial cells.Journal of cellular and molecular medicine · 2023Article
- A Lipid Perspective on Regulated Pyroptosis.International journal of biological sciences · 2023Review
- DNA methylation changes underlie the long-term association between periodontitis and atherosclerotic cardiovascular disease.Frontiers in cardiovascular medicine · 2023Article
- Review
- The Regulation of Pyroptosis and Ferroptosis by MicroRNAs in Cardiovascular Diseases.Galen medical journal · 2023Article
- The emerging role of pyroptosis-related inflammasome pathway in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2022Review
- Chronic apical periodontitis exacerbates atherosclerosis in apolipoprotein E-deficient mice and leads to changes in the diversity of gut microbiota.International endodontic journal · 2022Article
- Porphyromonas gingivalis outside the oral cavity.Odontology · 2022Review
- PAMPs and DAMPs as the Bridge Between Periodontitis and Atherosclerosis: The Potential Therapeutic Targets.Frontiers in cell and developmental biology · 2022Review
- Emerging Roles of Inflammasomes in Cardiovascular Diseases.Frontiers in immunology · 2022Review
- Pyroptosis-Mediated Periodontal Disease.International journal of molecular sciences · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
There is strong epidemiological association between periodontal disease and cardiovascular disease but underlying mechanisms remain ill-defined. Because the human periodontal disease pathogen, Porphyromonas gingivalis (Pg), interacts with innate immune receptors Toll-like Receptor (TLR) 2 and CD36/scavenger receptor-B2 (SR-B2), we studied how CD36/SR-B2 and TLR pathways promote Pg-mediated atherosclerosis. Western diet fed low density lipoprotein receptor knockout (Ldlr°) mice infected orally with Pg had a significant increase in lesion burden compared with uninfected controls.This increase was entirely CD36/SR-B2-dependent, as there was no significant change in lesion burden between infected and uninfected Cd36o/Ldlro mice [corrected]. Western diet feeding promoted enhanced CD36/SR-B2-dependent IL1β generation and foam cell formation as a result of Pg lipopolysaccharide (PgLPS) exposure. CD36/SR-B2 and TLR2 were necessary for inflammasome activation and optimal IL1ß generation, but also resulted in LPS induced lethality (pyroptosis). Modified forms of LDL inhibited Pg-mediated IL1ß generation in a CD36/SR-B2-dependent manner and prevented pyroptosis, but promoted foam cell formation. Our data show that Pg infection in the oral cavity can lead to significant TLR2-CD36/SR-B2 dependent IL1ß release. In the vessel wall, macrophages encountering systemic release of IL1ß, PgLPS and modified LDL have increased lipid uptake, foam cell formation, and release of IL1ß, but because pyroptosis is inhibited, this enables macrophage survival and promotes increased plaque development. These studies may explain increased lesion burden as a result of periodontal disease, and suggest strategies for development of therapeutics.
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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.