ArticleDisease markers2015
Toll-Like Receptor 9 Inactivation Alleviated Atherosclerotic Progression and Inhibited Macrophage Polarized to M1 Phenotype in ApoE-/- Mice.
Article in Disease markers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 40 citations in OpenAlex.
- The TLR9 Agonist Cobitolimod Induces IL10-Producing Wound Healing Macrophages and Regulatory T Cells in Ulcerative Colitis.Journal of Crohn's & colitis · 2020Trial
- Toll-like receptor 9 promotes aortic chondrogenesis and calcification in apolipoprotein E-deficient mice.Heart and vessels · 2026Article
- The role of interferon regulatory factors in atherosclerosis: from cell type-specific mechanisms to therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Chronic intermittent hypoxia drives M1 macrophage polarization in dorsal root ganglia.Brain, behavior, and immunity · 2025Article
- The role of intestinal macrophage polarization in colitis-associated colon cancer.Frontiers in immunology · 2025Review
- Review
- Cigarette Smoking and Atherosclerotic Cardiovascular Disease.Journal of atherosclerosis and thrombosis · 2024Review
- Emerging Roles of the Innate Immune System Regulated by DNA Sensors in the Development of Vascular and Metabolic Diseases.Journal of atherosclerosis and thrombosis · 2022Review
- Endothelial cells: potential novel regulators of renal inflammation.American journal of physiology. Renal physiology · 2022Review
- Circulating Mitochondrial DNA and Inter-Organelle Contact Sites in Aging and Associated Conditions.Cells · 2022Review
- Expanding role of deoxyribonucleic acid-sensing mechanism in the development of lifestyle-related diseases.Frontiers in cardiovascular medicine · 2022Review
- Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Review
- Innate Immune Receptors, Key Actors in Cardiovascular Diseases.JACC. Basic to translational science · 2020Review
- The Role of Toll-like Receptors in Atherothrombotic Cardiovascular Disease.ACS pharmacology & translational science · 2020Review
- Emerging roles of Toll-like receptor 9 in cardiometabolic disorders.Inflammation and regeneration · 2020Review
- Pharmacological modulation of nucleic acid sensors - therapeutic potential and persisting obstacles.Nature reviews. Drug discovery · 2019Review
- Toll-Like Receptor 9 Plays a Pivotal Role in Angiotensin II-Induced Atherosclerosis.Journal of the American Heart Association · 2019Article
- Suppression of Gut Bacterial Translocation Ameliorates Vascular Calcification through Inhibiting Toll-Like Receptor 9-Mediated BMP-2 Expression.Oxidative medicine and cellular longevity · 2019Article
- RAGE and TLRs as Key Targets for Antiatherosclerotic Therapy.BioMed research international · 2018Review
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveToll-like receptor 9 (TLR9) is involved in many inflammatory diseases, but its role in atherosclerosis remains controversial. This study aimed to investigate the role of TLR9 in atherosclerosis development and macrophage polarization.
methodsApoE(-/-) mice were treated with vehicle or IRS869 for 12 weeks. Plaque vulnerability was assessed with immunohistochemical analysis, picro-sirius red, and oil red O staining. The expressions of M1- and M2-associated markers in plaques were detected by RT-PCR and immunofluorescence. The aorta TLR9 and its downstream molecules including myeloid differentiation protein 88 (MyD88), phosphorylated nuclear factor-kappa B (p-NF-κB), and interferon regulatory factor 7 (IRF7) were determined by western blot analysis. The frequency of M1 and M2 subtype in RAW264.7 cells treated with IRS869 and/or ODN1826 was evaluated with flow cytometry.
resultsIn ApoE(-/-) mice, functional inactivation of TLR9 pathway resulted in attenuated atherosclerosis development, as manifested by reduced plaque burden and by decreased plaque vulnerability. Mechanistically, TLR9 inhibition prevented the activation of MyD88/NF-κB pathway and shifted the balance of M1/M2 toward M2 macrophages that were involved.
conclusionsOur data indicated that TLR9 inactivation ameliorated atherosclerosis via skewing macrophage plasticity to M2 phenotype in ApoE-deficient mice. These findings may provide a promising therapeutic strategy for atherosclerosis.
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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.