ArticlePloS one2016
Toll-Like Receptor 4 Is Essential in the Development of Abdominal Aortic Aneurysm.
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.
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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, 52 citations in OpenAlex.
- Alginate oligosaccharide indirectly affects toll-like receptor signaling via the inhibition of microRNA-29b in aneurysm patients after endovascular aortic repair.Drug design, development and therapy · 2017Trial
- Abdominal aortic aneurysm progression: A review of preclinical and clinical data.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Review
- Knockdown of GBP5 Attenuates Abdominal Aortic Aneurysm Formation via the NF-κB Pathway.Applied biochemistry and biotechnology · 2026Article
- HDL in Abdominal Aortic Aneurysm: Mechanistic Insight and Therapeutic Potential.Current atherosclerosis reports · 2026Review
- The Association Between Serum HMGB2 Levels and Abdominal Aortic Aneurysm in Males: Insights Into the HMGB2-TREM Pathway.Reviews in cardiovascular medicine · 2025Article
- Article
- Review
- Treatment With Small Molecule Inhibitors of Advanced Glycation End-Products Formation and Advanced Glycation End-Products-Mediated Collagen Cross-Linking Promotes Experimental Aortic Aneurysm Progression in Diabetic Mice.Journal of the American Heart Association · 2023Article
- Dexmedetomidine protects cells from Angiotensin II-induced smooth muscle cell phenotype switch and endothelial cell dysfunction.Cell cycle (Georgetown, Tex.) · 2023Article
- Soluble CD93 lectin-like domain sequesters HMGB1 to ameliorate inflammatory diseases.Theranostics · 2023Article
- The role of phosphoinositide 3-kinases in immune-inflammatory responses: potential therapeutic targets for abdominal aortic aneurysm.Cell cycle (Georgetown, Tex.) · 2022Review
- MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021Review
- Angiotensin-converting enzyme 2, coronavirus disease 2019, and abdominal aortic aneurysms.Journal of vascular surgery · 2021Review
- The elevated expression of TLR4 and MMP9 in human abdominal aortic aneurysm tissues and its implication.BMC cardiovascular disorders · 2021Article
- Resistin induces cardiac fibroblast-myofibroblast differentiation through JAK/STAT3 and JNK/c-Jun signaling.Pharmacological research · 2021Article
- Daphnetin suppresses experimental abdominal aortic aneurysms in mice via inhibition of aortic mural inflammation.Experimental and therapeutic medicine · 2020Article
- Lung-derived HMGB1 is detrimental for vascular remodeling of metabolically imbalanced arterial macrophages.Nature communications · 2020Article
- Adult mouse hippocampal transcriptome changes associated with long-term behavioral and metabolic effects of gestational air pollution toxicity.Translational psychiatry · 2020Article
- DAPT, a potent Notch inhibitor regresses actively growing abdominal aortic aneurysm via divergent pathways.Clinical science (London, England : 1979) · 2020Article
- Insight into the expression of toll-like receptors 2 and 4 in patients with abdominal aortic aneurysm.Molecular biology reports · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor (TLR) family plays a key role in innate immunity and various inflammatory responses. TLR4, one of the well-characterized pattern-recognition receptors, can be activated by endogenous damage-associated molecular pattern molecules such as high mobility group box 1 (HMGB1) to sustain sterile inflammation. Evidence suggested that blockade of TLR4 signaling may confer protection against abdominal aortic aneurysm (AAA). Herein we aimed to obtain further insight into the mechanism by which TLR4 might promote aneurysm formation. Characterization of the CaCl2-induced AAA model in mice revealed that upregulation of TLR4 expression, localized predominantly to vascular smooth muscle cells (VSMCs), was followed by a late decline during a 28-day period of AAA development. In vitro, TLR4 expression was increased in VSMCs treated with HMGB1. Knockdown of TLR4 by siRNA attenuated HMGB1-enhanced production of proinflammatory cytokines, specifically interleukin-6 and monocyte chemoattractant protein-1 (MCP-1), and matrix-degrading matrix metalloproteinase (MMP)-2 from VSMCs. In vivo, two different strains of TLR4-deficient (C57BL/10ScNJ and C3H/HeJ) mice were resistant to CaCl2-induced AAA formation compared to their respective controls (C57BL/10ScSnJ and C3H/HeN). Knockout of TLR4 reduced interleukin-6 and MCP-1 levels and HMGB1 expression, attenuated macrophage accumulation, and eventually suppressed MMP production, elastin destruction and VSMC loss. Finally, human AAA exhibited higher TLR4 expression that was localized to VSMCs. These data suggest that TLR4 signaling contributes to AAA formation by promoting a proinflammatory status of VSMCs and by inducing proteinase release from VSMCs during aneurysm initiation and development.
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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.