Neutrophil Extracellular Traps in Atherosclerosis and Thrombosis

Hofbauer, Thomas M.; Ondracek, Anna S.; Lang, Irene

doi:10.1007/164_2020_409

Cited by 14 publications

(13 citation statements)

References 143 publications

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“…At the same time, NETs also promote the abnormal activation of macrophages and upregulate the levels of IL-8 and inflammasomes, thereby further amplifying the role of NETs and accelerating the progression of atherosclerosis (23,(29)(30)(31). Macrophages are more common in the types of lesions that are prone to rupture, but studies have shown that the infiltration of neutrophils is more important for these erosion-prone lesions (32). Oxidized low-density lipoprotein (oxLDL), which easily accumulates in macrophages, is used as an atherosclerosisinducing molecule.…”

Section: Nets In Atherosclerosismentioning

confidence: 99%

The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

Zhou

Tao

Shen

et al. 2021

Front. Cardiovasc. Med.

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Neutrophils play a vital role in the formation of arterial, venous and cancer-related thrombosis. Recent studies have shown that in a process known as NETosis, neutrophils release proteins and enzymes complexed to DNA fibers, collectively called neutrophil extracellular traps (NETs). Although NETs were originally described as a way for the host to capture and kill bacteria, current knowledge indicates that NETs also play an important role in thrombosis. According to recent studies, the destruction of vascular microenvironmental homeostasis and excessive NET formation lead to pathological thrombosis. In vitro experiments have found that NETs provide skeletal support for platelets, red blood cells and procoagulant molecules to promote thrombosis. The protein components contained in NETs activate the endogenous coagulation pathway to promote thrombosis. Therefore, NETs play an important role in the formation of arterial thrombosis, venous thrombosis and cancer-related thrombosis. This review will systematically summarize and explain the study of NETs in thrombosis in animal models and in vivo experiments to provide new targets for thrombosis prevention and treatment.

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Section: Nets In Atherosclerosismentioning

confidence: 99%

The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

Zhou

Tao

Shen

et al. 2021

Front. Cardiovasc. Med.

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“…Neutrophils are the most abundant leukocytes in peripheral blood and one of the first innate immune cells to arrive at the site of inflammation ( 14 ). Neutrophils contribute to the occurrence and progression of atherosclerosis by releasing granular proteins such as matrix metalloproteinase ( 15 , 16 ), myeloperoxidase ( 17 , 18 ), elastase ( 19 ) and forming neutrophil extracellular traps (NETs) ( 20 , 21 ). There are a growing body of evidences suggesting that neutrophils have a highly variable transcriptome profile depending on their tissue location and microenvironment ( 22 ).…”

Section: Introductionmentioning

confidence: 99%

Antigen-Presenting Cell-Like Neutrophils Foster T Cell Response in Hyperlipidemic Patients and Atherosclerotic Mice

Zhao

Jiang

et al. 2022

Front. Immunol.

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Neutrophils constitute abundant cellular components in atherosclerotic plaques. Most of the current studies are focused on the roles of granular proteins released by neutrophils in atherosclerosis. Here, we revealed a unique subset of neutrophils which exhibit the characteristics of antigen-presenting cell (APC) (which were called APC-like neutrophils afterwards) in atherosclerosis. The roles of APC-like neutrophils and relevant mechanisms were investigated in hyperlipidemic patients and atherosclerotic mice. Higher percentages of neutrophils and APC-like neutrophils were found in peripheral blood of hyperlipidemic patients than that of healthy donors. Meanwhile, we also identified higher infiltration of neutrophils and APC-like neutrophils in atherosclerotic mice. Ox-LDL induced Phorbol-12-myristate-13-acetate (PMA)-activated neutrophils to acquire the APC-like phenotype. Importantly, upon over-expression of APC-like markers, neutrophils acquired APC functions to promote the proliferation and interferon-γ production of CD3+ T cells via HLA-DR/CD80/CD86. In accordance with what found in vitro, positive correlation between neutrophils and CD3+ T cells was observed in hyperlipidemic patients. In conclusion, our work identifies a proinflammatory neutrophil subset in both hyperlipidemic patients and atherosclerotic mice. This unique phenotype of neutrophils could activate the adaptive immune response to promote atherosclerosis progression. Thus, this neutrophil subset may be a new target for immunotherapy of atherosclerosis.

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“… 16 One potential mechanism may be NETosis, the release of so‐called neutrophil extracellular traps (NETs) by neutrophils upon activation by platelets and inflammatory cytokines upstream of CRP. 17 Overactive NETosis may have detrimental effects in a variety of clinical scenarios such as atherothrombosis 18 and has been detected in coronary thrombi. 19 , 20 …”

Section: Discussionmentioning

confidence: 99%

Association of Periprocedural Inflammatory Activation With Increased Risk for Early Coronary Stent Thrombosis

Krychtiuk,

Bräu,

Schauer

et al. 2024

JAHA

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Background Stent thrombosis is a rare but deleterious event. Routine coronary angiography with percutaneous coronary intervention (PCI) is often deferred in the presence of laboratory markers of acute inflammation to prevent complications. The aim of this study was to investigate whether an acute inflammatory state is associated with an increased risk of early stent thrombosis. Methods and Results Within a prospective single‐center registry, the association between preprocedural acute inflammatory activation, defined as C‐reactive protein plasma levels >50 mg/L or a leukocyte count >12 g/L, and occurrence of early (≤30 days) stent thrombosis was evaluated. In total, 11 327 patients underwent PCI and of those, 6880 patients had laboratory results available. 49.6% of the study population received PCI for an acute coronary syndrome and 50.4% for stable ischemic heart disease. In patients with signs of acute inflammatory activation (24.9%), PCI was associated with a significantly increased risk for stent thrombosis (hazard ratio, 2.89; P <0.00001), independent of age, sex, kidney function, number and type of stents, presence of multivessel disease, choice of P2Y12 inhibitor, and clinical presentation. Elevated laboratory markers of acute inflammation were associated with the occurrence of stent thrombosis in both patients with acute coronary syndrome (hazard ratio, 2.63; P <0.001) and in patients with stable ischemic heart disease (hazard ratio, 3.57; P <0.001). Conclusions An acute inflammatory state at the time of PCI was associated with a significantly increased risk of early stent thrombosis. Evidence of acute inflammation should result in deferred PCI in elective patients, while future studies are needed for patients with acute coronary syndrome.

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Neutrophil Extracellular Traps in Atherosclerosis and Thrombosis

Cited by 14 publications

References 143 publications

The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

Antigen-Presenting Cell-Like Neutrophils Foster T Cell Response in Hyperlipidemic Patients and Atherosclerotic Mice

Association of Periprocedural Inflammatory Activation With Increased Risk for Early Coronary Stent Thrombosis

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