ArticleJCI insight2021
Angiotensin II triggers release of neutrophil extracellular traps, linking thromboinflammation with essential hypertension.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 92 citations in OpenAlex.
- Neutrophil extracellular traps in cardiovascular disease: Mechanisms and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Mechanism-Driven Design of Metal-Phenolic Networks: From Precision Assembly to Multidimensional Synergistic Therapy for Brain Diseases.Pharmaceutics · 2026Review
- Emerging evidence of neutrophil extracellular traps in essential hypertension and target organ damage: pathophysiological insights and therapeutic implications.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- LL-37 IgG levels are associated with clinical characteristics and T follicular cell response in acute coronary syndrome in adults.Physiological reports · 2026Article
- Mapping benefit, risk, and opportunity in PAD4 inhibition.Frontiers in immunology · 2026Review
- Inflammatory responses driven by neutrophil extracellular traps in cardiovascular diseases: molecular mechanisms, emerging biomarkers, and therapeutic targets.Frontiers in immunology · 2026Review
- NETosis in myocardial ischemia-reperfusion injury: From mechanisms to therapies (Review).Biomedical reports · 2025Review
- Neutrophil extracellular traps in cancer: From mechanisms to treatments.Clinical and translational medicine · 2025Review
- Imaging of Thromboinflammation by MultispectralInternational journal of molecular sciences · 2025Review
- Therapeutic Strategies for MASH: An Update on Drug Candidates Under Investigation in Late-Phase Clinical Trials.International journal of translational medicine (Basel, Switzerland) · 2025Article
- Recent advances on immunity and hypertension: the new cells on the kidney block.American journal of physiology. Renal physiology · 2025Review
- Pathophysiological Role of Neutrophil Extracellular Traps in Diet-Induced Obesity and Metabolic Syndrome in Animal Models.Nutrients · 2025Review
- Neutrophil extracellular traps as therapeutics target in vascular aging.Frontiers in immunology · 2025Review
- The Role of Neutrophil Extracellular Traps in Atherosclerosis: From the Molecular to the Clinical Level.Journal of inflammation research · 2025Review
- Role of Neutrophil Extracellular Traps in Hypertension and Their Impact on Target Organs.Journal of clinical hypertension (Greenwich, Conn.) · 2025Review
- The interplay of ferroptosis and oxidative stress in the pathogenesis of aortic dissection.Frontiers in pharmacology · 2025Review
- Predictive role of neutrophil percentage-to-albumin ratio, neutrophil-to-lymphocyte ratio, and systemic immune-inflammation index for mortality in patients with MASLD.Scientific reports · 2024Article
- Neutrophil extracellular traps: a catalyst for atherosclerosis.Molecular and cellular biochemistry · 2024Review
- Improvement of the Immunity System Through Sports: Novel Regulatory Mechanisms for Hypertension.Reviews in cardiovascular medicine · 2024Review
- Highly sensitive magnetic particle imaging of abdominal aortic aneurysm NETosis with anti-Ly6G iron oxide nanoparticles.Cell death discovery · 2024Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Innate immunity and chronic inflammation are involved in atherosclerosis and atherothrombosis, leading to target organ damage in essential hypertension (EH). However, the role of neutrophils in EH is still elusive. We investigated the association between angiotensin II (Ang II) and neutrophil extracellular traps (NETs) in pathogenesis of EH. Plasma samples, kidney biopsies, and surgical specimens of abdominal aortic aneurysms (AAAs) from patients with EH were used. Cell-based assays, NETs/human aortic endothelial cell cocultures, and in situ studies were performed. Increased plasma levels of NETs and tissue factor (TF) activity were detected in untreated, newly diagnosed patients with EH. Stimulation of control neutrophils with plasma from patients with untreated EH generated TF-enriched NETs promoting endothelial collagen production. Ang II induced NETosis in vitro via an ROS/peptidylarginine deiminase type 4 and autophagy-dependent pathway. Circulating NETs and thrombin generation levels were reduced substantially in patients with EH starting treatment with Ang II receptor blockers, whereas their plasma was unable to trigger procoagulant NETs. Moreover, TF-bearing NETotic neutrophils/remnants accumulated in sites of interstitial renal fibrosis and in the subendothelial layer of AAAs. These data reveal the important pathogenic role of an Ang II/ROS/NET/TF axis in EH, linking thromboinflammation with endothelial dysfunction and fibrosis.
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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.