ArticleAtherosclerosis2013
TLR3 deficiency protects against collagen degradation and medial destruction in murine atherosclerotic plaques.
Article in Atherosclerosis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 41 citations in OpenAlex.
- The Role of Toll-like Receptors and Viral Infections in the Pathogenesis and Progression of Pulmonary Arterial Hypertension-A Narrative Review.International journal of molecular sciences · 2025Review
- The Role of TLRs in Obesity and Its Related Metabolic Disorders.International journal of molecular sciences · 2025Review
- Desipramine enhances the stability of atherosclerotic plaque in rabbits monitored with molecular imaging.PloS one · 2023Article
- Small molecule SMU-CX24 targeting toll-like receptor 3 counteracts inflammation: A novel approach to atherosclerosis therapy.Acta pharmaceutica Sinica. B · 2022Article
- Elevated granulocyte-colony stimulating factor and hematopoietic stem cell mobilization in Niemann-Pick type C1 disease.Journal of lipid research · 2022Article
- Review
- Infection and atherosclerosis: TLR-dependent pathways.Cellular and molecular life sciences : CMLS · 2020Review
- The Role of Toll-like Receptors in Atherothrombotic Cardiovascular Disease.ACS pharmacology & translational science · 2020Review
- Sex as a Biological Variable in Atherosclerosis.Circulation research · 2020Review
- Toll-like Receptors as a Potential Drug Target for Diabetes Mellitus and Diabetes-associated Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
- Modulation of Immune-Inflammatory Responses in Abdominal Aortic Aneurysm: Emerging Molecular Targets.Journal of immunology research · 2018Review
- Toll-like receptor 7 deficiency protects apolipoprotein E-deficient mice from diet-induced atherosclerosis.Scientific reports · 2017Article
- Inhibition of Toll-Like Receptor Signaling as a Promising Therapy for Inflammatory Diseases: A Journey from Molecular to Nano Therapeutics.Frontiers in physiology · 2017Review
- Smooth Muscle Cell-Derived Interleukin-17C Plays an Atherogenic Role via the Recruitment of Proinflammatory Interleukin-17A+ T Cells to the Aorta.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Hyperglycemia Suppresses Calcium Phosphate-Induced Aneurysm Formation Through Inhibition of Macrophage Activation.Journal of the American Heart Association · 2016Article
- Toll-like Receptors in the Vascular System: Sensing the Dangers Within.Pharmacological reviews · 2016Review
- Activation of Toll-like receptor 3 increases mouse aortic vascular smooth muscle cell contractility through ERK1/2 pathway.Pflugers Archiv : European journal of physiology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveInflammatory cell activation plays a key role in atherosclerotic plaque growth and acute complications. While secretion of proteases and inflammatory cytokines are likely involved in the development of plaque instability, the precise mechanistic pathways are not well understood. METHODS AND
resultsBased on our previous study, we crossed Toll-like receptor 3 (Tlr3)(-/-) mice with a unique BALB-Apoe(-/-)Npc1(-/-) plaque complication-susceptible mouse model, as well as the widely-used B6-Ldlr(-/-) atherosclerosis model, to test the role of TLR3 signaling in the development of plaque instability. TLR3-deficient mice showed no change in aortic root lesion area, but displayed a marked increase in collagen and smooth muscle cell (SMC) content of lesions. Notably, Apoe(-/-)Npc1(-/-)Tlr3(-/-) mice exhibited a 50% reduction in the incidence of medial destruction, a precursor to aortic aneurysm formation. MMP-2 activity was markedly reduced in aortic extracts from Apoe(-/-)Npc1(-/-)Tlr3(-/-) compared to controls, while both MMP-2 and -9 activities were reduced in Ldlr(-/-)Tlr3(-/-) extracts. Consistent with the in vivo data, TLR3 deficiency suppressed MMP-2 activity induced by TNF-α or polyinosine-polycytidylic acid in macrophages from Apoe(-/-)Npc1(-/-) mice.
conclusionsTLR3 plays a critical role in regulating the degradation of extracellular matrix in lesions, in part by modulation of macrophage MMP-2 and -9 activities.
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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.