ArticleEuropean heart journal2015
TLR2 and neutrophils potentiate endothelial stress, apoptosis and detachment: implications for superficial erosion.
Article in European heart journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers.
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Who cites it
192 citing papers in PubMed, 372 citations in OpenAlex.
- Physical exertion as a trigger of acute coronary syndrome caused by plaque erosion.Journal of thrombosis and thrombolysis · 2020Trial
- Myeloid TLR2 signaling amplifies immunopathology in influenza-infected murine neonates.American journal of respiratory cell and molecular biology · 2026Article
- Bioinspired nanoparticles deliver DNase I to attenuate ulcerative colitis by degrading NETs and modulating PTGS2-mediated ER stress.Materials today. Bio · 2026Article
- Review
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- Combined value of AIP and NHR for identifying obstructive coronary heart disease in premature cases with zero calcium.BMC cardiovascular disorders · 2026Article
- Local to Systemic Inflammation-From Generation to Prognosis in Acute Coronary Syndrome.Biomedicines · 2026Review
- Neutrophil redox imbalance in acute coronary syndrome.Journal of medical biochemistry · 2026Article
- Pathogenesis of plaque erosion.Trends in cardiovascular medicine · 2026Review
- Spatiotemporal dynamics of tumor-associated neutrophils: bridging the gap between cancer progression and immunotherapy.Molecular cancer · 2026Review
- Intra-coronary imaging and transcriptomics of calcified nodules before and after intensive lipid-lowering therapy: a YELLOW III substudy.European heart journal. Imaging methods and practice · 2026Article
- Citrullination Accompanies the Development of Carotid Atherosclerotic Plaques.Current medicinal chemistry · 2026Article
- Neutrophil Extracellular Traps-Mediated Intraplaque Angiogenesis and Microvascular Permeability Promote Rapid Plaque Progression following Myocardial Infarction.Research (Washington, D.C.) · 2026Article
- Neutrophil Extracellular Traps (NETs) in health and disease.Molecular biomedicine · 2025Review
- Current status and challenges of multi-omics research using animal models of atherosclerosis.Journal of molecular and cellular cardiology plus · 2025Review
- Cigarette Tar Enhanced ECs Pyroptosis via CAMKII/Drp1/mtDNA: Novel Insight Into the Mechanism of Plaque Erosion.JACC. Basic to translational science · 2025Article
- Acute coronary syndromes: mechanisms, challenges, and new opportunities.European heart journal · 2025Review
- Upregulation of TLR-MYD88 signaling, stem cell genes, and Klotho mediates sepsis-associated myocardial inflammation.Molecular biology reports · 2025Article
- Biomarkers Differentiating Plaque Erosion from Stable Plaque.Current atherosclerosis reports · 2025Review
- Inflammatory Pathways in Coronary Artery Disease: Which Ones to Target for Secondary Prevention?Cells · 2025Review
132 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsSuperficial erosion of atheromata causes many acute coronary syndromes, but arises from unknown mechanisms. This study tested the hypothesis that Toll-like receptor-2 (TLR2) activation contributes to endothelial apoptosis and denudation and thus contributes to the pathogenesis of superficial erosion. METHODS AND
resultsToll-like receptor-2 and neutrophils localized at sites of superficially eroded human plaques. In vitro, TLR2 ligands (including hyaluronan, a matrix macromolecule abundant in eroded lesions) induced endothelial stress, characterized by reactive oxygen species production, endoplasmic reticulum (ER) stress, and apoptosis. Co-incubation of neutrophils with endothelial cells (ECs) potentiated these effects and induced EC apoptosis and detachment. We then categorized human atherosclerotic plaques (n = 56) based on morphologic features associated with superficial erosion, 'stable' fibrotic, or 'vulnerable' lesions. Morphometric analyses of the human atheromata localized neutrophils and neutrophil extracellular traps (NETs) near clusters of apoptotic ECs in smooth muscle cell (SMC)-rich plaques. The number of luminal apoptotic ECs correlated with neutrophil accumulation, amount of NETs, and TLR2 staining in SMC-rich plaques, but not in 'vulnerable' atheromata.
conclusionThese in vitro observations and analyses of human plaques indicate that TLR2 stimulation followed by neutrophil participation may render smooth muscle cell-rich plaques susceptible to superficial erosion and thrombotic complications by inducing ER stress, apoptosis, and favouring detachment of EC.
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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.