The Role of Neutrophils in Hypertension

Araos, Patricio; Figueroa, Stefanny; Amador, Cristián A.

doi:10.3390/ijms21228536

Cited by 34 publications

(28 citation statements)

References 97 publications

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“…In this context, neutrophils are also considered as the major effector of tissue damage in both atherosclerosis and CV risk factor-associated end-organ damage, where dysfunctional endothelial cells allow for increased neutrophils’ intravascular activation and their translocation to tissues [ 34 , 35 ]. The role of neutrophils in tissue damage is associated with many tissue devastating mechanisms that are inherent to their function, including release of a large amount of pro-inflammatory cytokines, proteolytic and oxidizing enzymes, and reactive oxidative species (ROS) [ 36 ].…”

Section: Proposed Underlying Mechanisms Of Differences Between Men and Women In Cardiovascular Disease Patternsmentioning

confidence: 99%

“…Growing evidence indicates also the role of neutrophils in both, the development and the progression of atherosclerotic lesions, and plaque destabilization and rupture. Emerging evidence indicates the critical role of neutrophils in CV risk factor-related target-organ disease ( Figure 1 ) [ 34 ]. This role of neutrophils is associated with their increased recruitment from the circulation by dysfunctional endothelium and prolonged persistence in tissue, due to decreased apoptosis and disturbed clearance by macrophages [ 35 , 43 ].…”

Section: Leukocyte Counts and Ratios As Markers Of Inflammation In Cardiovascular Diseasementioning

confidence: 99%

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Neutrophil-to-Lymphocyte Ratio as a Cardiovascular Risk Marker May Be Less Efficient in Women Than in Men

et al. 2021

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Cardiovascular disease (CVD) is the leading cause of death in women, although traditionally, it has been considered as a male dominated disease. Chronic inflammation plays a crucial role in the development of insulin resistance, diabetes type 2 and CVD. Since studies on women were scarce, in order to improve diagnosis and treatment of CVD, there is a need to improve understanding of the role of inflammation in the development of CVD in women. The neutrophil-to-lymphocyte ratio (NLR) is an inexpensive and widely available marker of inflammation, and has been studied in cardio-metabolic disorders. There is a paucity of data on sex specific differences in the lifetime course of NLR. Men and women differ to each other in sex hormones and characteristics of immune reaction and the expression of CVD. These factors can determine NLR values and their variations along the life course. In particular, menopause in women is a period associated with profound physiological and hormonal changes, and is coincidental with aging. An emergence of CV risk factors with aging, and age-related changes in the immune system, are factors that are associated with an increase in prevalence of CVD in both sexes. The aim of this review is to comprehend the available evidence on this issue, and to discuss sex specific differences in the lifetime course of NLR in the light of immune and inflammation mechanisms.

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Section: Proposed Underlying Mechanisms Of Differences Between Men and Women In Cardiovascular Disease Patternsmentioning

confidence: 99%

Section: Leukocyte Counts and Ratios As Markers Of Inflammation In Cardiovascular Diseasementioning

confidence: 99%

Neutrophil-to-Lymphocyte Ratio as a Cardiovascular Risk Marker May Be Less Efficient in Women Than in Men

et al. 2021

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“…Moreover, in addition to elevated neutrophil counts, hypertensive patients also show unleashed neutrophil responses that can modulate the microenvironment in blood vessels. Neutrophils could, in turn, mediate vascular damage and promote endothelial cell death by secreting ROS, which could ultimately make them active participants in the development of arterial hypertension [204].…”

Section: Nets and Hypertensionmentioning

confidence: 99%

Contemporary Lifestyle and Neutrophil Extracellular Traps: An Emerging Link in Atherosclerosis Disease

Pérez-Olivares¹,

Soehnlein

2021

Cells

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Neutrophil extracellular traps (NETs) are networks of extracellular genetic material decorated with proteins of nuclear, granular and cytosolic origin that activated neutrophils expel under pathogenic inflammatory conditions. NETs are part of the host’s innate immune defense system against invading pathogens. Interestingly, these extracellular structures can also be released in response to sterile inflammatory stimuli (e.g., shear stress, lipidic molecules, pro-thrombotic factors, aggregated platelets, or pro-inflammatory cytokines), as in atherosclerosis disease. Indeed, NETs have been identified in the intimal surface of diseased arteries under cardiovascular disease conditions, where they sustain inflammation via NET-mediated cell-adhesion mechanisms and promote cellular dysfunction and tissue damage via NET-associated cytotoxicity. This review will focus on (1) the active role of neutrophils and NETs as underestimated players of the inflammatory process during atherogenesis and lesion progression; (2) how these extracellular structures communicate with the main cell types present in the atherosclerotic lesion in the arterial wall; and (3) how these neutrophil effector functions interplay with lifestyle-derived risk factors such as an unbalanced diet, physical inactivity, smoking or lack of sleep quality, which represent major elements in the development of cardiovascular disease.

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“…Neutrophils represent the most abundant innate immune cells and through the secretion of several prooxidant and proinflammatory molecules are able to promote and facilitate immune-mediated inflammation at sites of tissue injury ( 7 ). However, even though epidemiological studies have correlated neutrophil count with increased risk of developing EH and kidney dysfunction ( 8 , 9 ), the experimental and clinical evidence regarding their exact role in the pathogenesis and complications of EH is limited ( 10 ).…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II triggers release of neutrophil extracellular traps, linking thromboinflammation with essential hypertension

Chrysanthopoulou¹,

Gkaliagkousi²,

Lazaridis³

et al. 2021

JCI Insight

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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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The Role of Neutrophils in Hypertension

Cited by 34 publications

References 97 publications

Neutrophil-to-Lymphocyte Ratio as a Cardiovascular Risk Marker May Be Less Efficient in Women Than in Men

Neutrophil-to-Lymphocyte Ratio as a Cardiovascular Risk Marker May Be Less Efficient in Women Than in Men

Contemporary Lifestyle and Neutrophil Extracellular Traps: An Emerging Link in Atherosclerosis Disease

Angiotensin II triggers release of neutrophil extracellular traps, linking thromboinflammation with essential hypertension

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