ArticleFrontiers in cell and developmental biology2022
Neutrophil extracellular traps-mediated Beclin-1 suppression aggravates atherosclerosis by inhibiting macrophage autophagy.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- Neutrophil extracellular traps in cardiovascular disease: Mechanisms and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Review
- The Interaction of Neutrophil Extracellular Traps and Complement in Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2026Review
- Neutrophil Extracellular Traps: Potential Therapeutic Targets of Traditional Chinese Medicine and Natural Products for Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Beclin 1 level combined with Gensini score and low-density lipoprotein cholesterol correlate strongly with multi-vessel disease.American journal of translational research · 2026Article
- Inflammatory responses driven by neutrophil extracellular traps in cardiovascular diseases: molecular mechanisms, emerging biomarkers, and therapeutic targets.Frontiers in immunology · 2026Review
- Comparative Analysis of Systemic Inflammatory Biomarkers Across Multiple Antiseizure Medications: A Single-Center Retrospective Cohort Study of 1782 Patients.Journal of clinical medicine · 2025Article
- Pilot Exploration of RGMa-BMP4 Signaling in Neutrophil Activation in NMOSD: Integrating Clinical and Molecular Insights.Molecular neurobiology · 2025Article
- Mechanism of Neutrophil p90RSK-Nrf2 Signaling Pathway in Atherosclerosis.Balkan medical journal · 2025Article
- BCL2A1‑ and G0S2‑driven neutrophil extracellular traps: A protective mechanism linking preeclampsia to reduced breast cancer risk.Oncology reports · 2025Article
- The Anti-Inflammatory Effects of Formononetin, an Active Constituent ofMolecules (Basel, Switzerland) · 2025Article
- The space-time continuum in neurological disorders of the autophagosome-lysosome fusion machinery.Autophagy reports · 2025Review
- The Role of Neutrophil Extracellular Traps in Atherosclerosis: From the Molecular to the Clinical Level.Journal of inflammation research · 2025Review
- Neutrophil extracellular traps: a catalyst for atherosclerosis.Molecular and cellular biochemistry · 2024Review
- HL-60 cells as a valuable model to study LPS-induced neutrophil extracellular traps release.Heliyon · 2024Article
- Neutrophil Extracellular Traps in Cardiovascular and Aortic Disease: A Narrative Review on Molecular Mechanisms and Therapeutic Targeting.International journal of molecular sciences · 2024Review
- Cigarette Smoking and Atherosclerotic Cardiovascular Disease.Journal of atherosclerosis and thrombosis · 2024Review
- The Role of Neutrophil Extracellular Traps in the Outcome of Malignant Epitheliomas: Significance of CA215 Involvement.Diagnostics (Basel, Switzerland) · 2024Review
- The expression of autophagy markers in IVIG-resistant Kawasaki disease and the establishment of prediction model.BMC pediatrics · 2023Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of evidence suggests that neutrophil extracellular traps (NETs) critically contribute to the development of atherosclerosis. However, the detailed mechanism of how NETs promote atherogenesis remains unknown. In this study, we explored the role of NETs for promoting atherosclerosis by modulating the activity of autophagy in macrophages. NETs were effectively induced by a nicotine administration to the HL-60 cell-derived neutrophil-like cells. Treatment with NETs markedly suppressed both autophagosome formation and autophagosome-lysosome fusion in 7-ketocholesterol-treated macrophages, which are accompanied by the enhancement of inflammasome activity. NETs upregulate epidermal growth factor receptor (EGFR) activity, which enhances Beclin-1 phosphorylation of the tyrosine residues of Beclin-1 by EGFR, inhibits the PI3 kinase activity of the Beclin1-Vps34 complex, and suppresses autophagosome formation in macrophages. Furthermore, NET-induced activation of EGFR allows Rubicon to increase its expression, thereby suppressing autophagosome-lysosome fusion.
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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.