ArticleInternational journal of oral science2023
Oral pathogen aggravates atherosclerosis by inducing smooth muscle cell apoptosis and repressing macrophage efferocytosis.
Article in International journal of oral science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 17 citations in OpenAlex.
- Non-Coding RNAs in Oral Diseases: From Pathogenesis to Clinical Translation.International journal of molecular sciences · 2026Review
- From Periodontal Pocket to Systemic Diseases: Mechanistic Insights Into the Role of Porphyromonas gingivalis in Host Pathology.Journal of cellular and molecular medicine · 2026Review
- Engineering etiology-aligned in vitro models of human vessels.Microsystems & nanoengineering · 2026Review
- Bacterial proteases and Bcl-2 proteins in peri-implant tissues: An exploratory cross-sectional study.Clinical oral investigations · 2026Article
- Decoding the Gut-Fat-Heart Axis: From Molecular Communication Networks to Clinical Translation Strategies.International journal of molecular sciences · 2026Review
- Study on the Effect and Mechanism of the Outer Membrane Vesicles ofMicroorganisms · 2026Article
- The macrophage polarization-ferroptosis axis as a therapeutically targetable immunometabolic framework in periodontitis.Frontiers in immunology · 2026Review
- Combined oral and peripheral blood detection ofJournal of oral microbiology · 2026Article
- Microbiota-Driven Immune Dysregulation Along the Gut-Lung-Vascular Axis in Asthma and Atherosclerosis.Biomedicines · 2025Review
- Edentulism as an independent risk factor for sarcopenia: evidence from cross-sectional and longitudinal analyses based on the CHARLS cohort.BMC oral health · 2025Article
- Ferroptosis and macrophage efferocytosis in periodontitis: Biological insights and therapeutic advances.Virulence · 2025Review
- Engineering Efferocytosis for Bone Regeneration.Macromolecular bioscience · 2025Review
- A Clinical Review of the Connections Between Diabetes Mellitus, Periodontal Disease, and Cardiovascular Pathologies.Biomedicines · 2025Review
- Porphyromonas gingivalis aggravates atherosclerotic plaque instability by promoting lipid-laden macrophage necroptosis.Signal transduction and targeted therapy · 2025Article
- Expression of miRNAs in the Relationship Between Periodontitis and Cardiovascular Diseases: A Systematic Review.Non-coding RNA · 2025Review
- Immune Regulation and Disulfidptosis in Atherosclerosis Influence Disease Progression and Therapy.Biomedicines · 2025Article
- Murine Models in Oral Research: A Narrative Review of Experimental Approaches and Cardiovascular Implications.Biology · 2025Review
- The oral-gut microbiota axis: a link in cardiometabolic diseases.NPJ biofilms and microbiomes · 2025Review
- Exercise in atherosclerosis: its beneficial effects and underlying mechanism.Frontiers in cell and developmental biology · 2025Review
- Extracellular Vesicles from Compression-Loaded Cementoblasts Promote the Tissue Repair Function of Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periodontitis imparting the increased risk of atherosclerotic cardiovascular diseases is partially due to the immune subversion of the oral pathogen, particularly the Porphyromonas gingivalis (P. gingivalis), by inducing apoptosis. However, it remains obscure whether accumulated apoptotic cells in P. gingivalis-accelerated plaque formation are associated with impaired macrophage clearance. Here, we show that smooth muscle cells (SMCs) have a greater susceptibility to P. gingivalis-induced apoptosis than endothelial cells through TLR2 pathway activation. Meanwhile, large amounts of miR-143/145 in P.gingivalis-infected SMCs are extracellularly released and captured by macrophages. Then, these miR-143/145 are translocated into the nucleus to promote Siglec-G transcription, which represses macrophage efferocytosis. By constructing three genetic mouse models, we further confirm the in vivo roles of TLR2 and miR-143/145 in P. gingivalis-accelerated atherosclerosis. Therapeutically, we develop P.gingivalis-pretreated macrophage membranes to coat metronidazole and anti-Siglec-G antibodies for treating atherosclerosis and periodontitis simultaneously. Our findings extend the knowledge of the mechanism and therapeutic strategy in oral pathogen-associated systemic diseases.
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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.