Endothelial Dysfunction Induced by Extracellular Neutrophil Traps Plays Important Role in the Occurrence and Treatment of Extracellular Neutrophil Traps-Related Disease

Yu, Shuyang; Liu, Jingyu; Yan, Nianlong

doi:10.3390/ijms23105626

Cited by 18 publications

(14 citation statements)

References 192 publications

(229 reference statements)

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“…It has been shown that NETs, apart from their beneficial role in clearing the invading microorganism, are implicated in the pathogenesis of many diseases in which endothelial dysfunction is present, such as sepsis and cardiovascular diseases. Therefore, there has been a growing interest in studying the role of NETs in endothelial dysfunction in sepsis ( 119 ). In vitro studies suggest that NETs can promote endothelial dysfunction, as indicated by increased endothelial expression of ICAM-1, VCAM-1, E-selectin, TF, and vWF ( 60 , 62 , 109 , 120 – 123 ).…”

Section: Neutrophils In Immunothrombosismentioning

confidence: 99%

Endothelial dysfunction and immunothrombosis in sepsis

et al. 2023

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Sepsis is a life-threatening clinical syndrome characterized by multiorgan dysfunction caused by a dysregulated or over-reactive host response to infection. During sepsis, the coagulation cascade is triggered by activated cells of the innate immune system, such as neutrophils and monocytes, resulting in clot formation mainly in the microcirculation, a process known as immunothrombosis. Although this process aims to protect the host through inhibition of the pathogen’s dissemination and survival, endothelial dysfunction and microthrombotic complications can rapidly lead to multiple organ dysfunction. The development of treatments targeting endothelial innate immune responses and immunothrombosis could be of great significance for reducing morbidity and mortality in patients with sepsis. Medications modifying cell-specific immune responses or inhibiting platelet–endothelial interaction or platelet activation have been proposed. Herein, we discuss the underlying mechanisms of organ-specific endothelial dysfunction and immunothrombosis in sepsis and its complications, while highlighting the recent advances in the development of new therapeutic approaches aiming at improving the short- or long-term prognosis in sepsis.

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Section: Neutrophils In Immunothrombosismentioning

confidence: 99%

Endothelial dysfunction and immunothrombosis in sepsis

et al. 2023

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“…myeloperoxidase-ANCA2 in most patients with MPA are positive which can be mainly evoked by the ANCA-mediated over-activation of neutrophils and release of inflammatory cytokines, reactive oxygen species and plasmin. [4] The excessive activation of neutrophils by ANCA could result in the formation of Neutrophil extracellular traps, which are involved not only in ANCA-mediated vascular injury but also in the production of ANCA itself. [5] The third mechanism refers to the anti-diuretic hormone theory proposed by Largeau et al, namely the overproduction of what is known as arginine vasopressin in humans.…”

Section: Discussionmentioning

confidence: 99%

A case report of posterior reversible encephalopathy syndrome caused by ANCA-associated vasculitis case report and retrospective analysis

et al. 2022

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Introduction: Posterior reversible encephalopathy syndrome is a reversible syndrome clinically manifested by significant variations in neuroimaging. Early treatment is indispensable to achieve the reversibility, which requires the punctual alleviation of its inducing factors.Patient concerns: Most symptoms of posterior reversible encephalopathy syndrome (PRES) patients can be dispelled followed by a good prognosis after the inducement removal. The patient died due to the untimely diagnosis and treatment of the primary disease. Therefore, sufficient attention should be paid to the PRES induced by ANCA-associated vasculitis (AAV). Diagnosis and interventions:The patient is a middle-aged male, with acute onset, previous history of hypertension, cholecystectomy, intestinal obstruction, spontaneous renal rupture, etc. For this complaint, the manifestations are mainly blurred vision with convulsion and transient disturbance of consciousness. In 1 day of treatment, these symptoms were relieved, and he was diagnosed as PRES combined with the cranial imaging. The AAV of the patient was confirmed by spleen pathology.Outcomes: Despite the relief of most symptoms in 1 day of symptomatic treatment, it is highly likely that the patient eventually died of AAV, it is highly likely that the patient eventually died of AAV which will invade the vascular system due to the failure to treat the primary disease in time.Lessons: For patients diagnosed as PRES, the punctual identification of cause should be performed, so as to diagnose and correct the cause and primary disease as soon as possible, accompanied with the dynamical observation of the relevant indicators for suspected patients to avoid systemic organ failure.Abbreviations: AAV = ANCA-associated vasculitis, ANCA = antineutrophil cytoplasmic antibody, CT = computed tomography, PRES = posterior reversible encephalopathy syndrome.

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“…These mechanisms result in collagen production and vascular injury. 43,44 Compelling evidence highlights the central role of T-cell activation, contributing to vascular alterations through the release of proinflammatory cytokines and organ damage. 36 Specifically, proinflammatory T cells, including CD4 + Th1 and Th17 cells, CD8 + T cells, and γδ-T cells have been documented in resistance vessels of patients with hypertension.…”

Section: Immune-mediated Responsesmentioning

confidence: 99%

Mechanisms of Vascular Inflammation and Potential Therapeutic Targets: A Position Paper From the ESH Working Group on Small Arteries

Rios,

de Ciuceis,

Georgiopoulos

et al. 2024

Hypertension

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Inflammatory responses in small vessels play an important role in the development of cardiovascular diseases, including hypertension, stroke, and small vessel disease. This involves various complex molecular processes including oxidative stress, inflammasome activation, immune-mediated responses, and protein misfolding, which together contribute to microvascular damage. In addition, epigenetic factors, including DNA methylation, histone modifications, and microRNAs influence vascular inflammation and injury. These phenomena may be acquired during the aging process or due to environmental factors. Activation of proinflammatory signaling pathways and molecular events induce low-grade and chronic inflammation with consequent cardiovascular damage. Identifying mechanism-specific targets might provide opportunities in the development of novel therapeutic approaches. Monoclonal antibodies targeting inflammatory cytokines and epigenetic drugs, show promise in reducing microvascular inflammation and associated cardiovascular diseases. In this article, we provide a comprehensive discussion of the complex mechanisms underlying microvascular inflammation and offer insights into innovative therapeutic strategies that may ameliorate vascular injury in cardiovascular disease.

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Endothelial Dysfunction Induced by Extracellular Neutrophil Traps Plays Important Role in the Occurrence and Treatment of Extracellular Neutrophil Traps-Related Disease

Cited by 18 publications

References 192 publications

Endothelial dysfunction and immunothrombosis in sepsis

Endothelial dysfunction and immunothrombosis in sepsis

A case report of posterior reversible encephalopathy syndrome caused by ANCA-associated vasculitis case report and retrospective analysis

Mechanisms of Vascular Inflammation and Potential Therapeutic Targets: A Position Paper From the ESH Working Group on Small Arteries

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