ArticlePloS one2016
Proinflammatory Stimulation of Toll-Like Receptor 9 with High Dose CpG ODN 1826 Impairs Endothelial Regeneration and Promotes Atherosclerosis in Mice.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Toll-like receptor 9 promotes aortic chondrogenesis and calcification in apolipoprotein E-deficient mice.Heart and vessels · 2026Article
- Mitochondria Activity and CXCR4 Collaboratively Promote the Differentiation of CD11cImmune network · 2024Article
- Triad3A-Mediated K48-Linked ubiquitination and degradation of TLR9 impairs mitochondrial bioenergetics and exacerbates diabetic cardiomyopathy.Journal of advanced research · 2024Article
- Cigarette Smoking and Atherosclerotic Cardiovascular Disease.Journal of atherosclerosis and thrombosis · 2024Review
- Regulation of toll-like receptor (TLR) signaling pathways in atherosclerosis: from mechanisms to targeted therapeutics.Acta pharmacologica Sinica · 2023Review
- Biodegradable scaffolds for enhancing vaccine delivery.Bioengineering & translational medicine · 2023Article
- Innate and adaptive AAV-mediated immune responses in a mouse model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2023Article
- 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
- Expanding role of deoxyribonucleic acid-sensing mechanism in the development of lifestyle-related diseases.Frontiers in cardiovascular medicine · 2022Review
- PAMPs and DAMPs as the Bridge Between Periodontitis and Atherosclerosis: The Potential Therapeutic Targets.Frontiers in cell and developmental biology · 2022Review
- Role of Mitochondria-Derived Danger Signals Released After Injury in Systemic Inflammation and Sepsis.Antioxidants & redox signaling · 2021Review
- Difluoromethylornithine (DFMO), an Inhibitor of Polyamine Biosynthesis, and AntioxidantInternational journal of molecular sciences · 2021Article
- Vascular Stress Signaling in Hypertension.Circulation research · 2021Review
- Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Article
- Review
- CpG-ODN-mediated TLR9 innate immune signalling and calcium dyshomeostasis converge on the NFκB inhibitory protein IκBβ to drive IL1α and IL1β expression.Immunology · 2020Article
- AIM2 Stimulation Impairs Reendothelialization and Promotes the Development of Atherosclerosis in Mice.Frontiers in cardiovascular medicine · 2020Article
- Overexpression of MicroRNA-16 Alleviates Atherosclerosis by Inhibition of Inflammatory Pathways.BioMed research international · 2020Article
- Emerging roles of Toll-like receptor 9 in cardiometabolic disorders.Inflammation and regeneration · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundToll-like receptors (TLR) of the innate immune system have been closely linked with the development of atherosclerotic lesions. TLR9 is activated by unmethylated CpG motifs within ssDNA, but also by CpG motifs in nucleic acids released during vascular apoptosis and necrosis. The role of TLR9 in vascular disease remains controversial and we sought to investigate the effects of a proinflammatory TLR9 stimulation in mice. METHODS AND
findingsTLR9-stimulation with high dose CpG ODN at concentrations between 6.25 nM to 30 nM induced a significant proinflammatory cytokine response in mice. This was associated with impaired reendothelialization upon acute denudation of the carotid and increased numbers of circulating endothelial microparticles, as a marker for amplified endothelial damage. Chronic TLR9 agonism in apolipoprotein E-deficient (ApoE-/-) mice fed a cholesterol-rich diet increased aortic production of reactive oxygen species, the number of circulating endothelial microparticles, circulating sca-1/flk-1 positive cells, and most importantly augmented atherosclerotic plaque formation when compared to vehicle treated animals. Importantly, high concentrations of CpG ODN are required for these proatherogenic effects.
conclusionsSystemic stimulation of TLR9 with high dose CpG ODN impaired reendothelialization upon acute vascular injury and increased atherosclerotic plaque development in ApoE-/- mice. Further studies are necessary to fully decipher the contradictory finding of TLR9 agonism in vascular biology.
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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.