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Updated: Jun 12, 2025
Neutrophil Lifespan Extension with CLON-G and an In Vitro Spontaneous Death Assay
Published on: May 12, 2023
Turning Neutrophil Cell Death Deadly in the Context of Hypertensive Vascular Disease
Sahand Salari Namin1, Yanfang Peipei Zhu2, Ben A Croker1
1Department of Pediatrics, University of California San Diego, La Jolla, California, USA.
Insights
Neutrophils and their extracellular traps (NETs) play a key role in hypertensive vascular disease (HVD). Targeting NET formation offers a promising therapeutic strategy for cardiovascular disorders.
Area of Science:
- Cardiovascular Science
- Immunology
- Pathology
Background:
- Hypertensive vascular disease (HVD) is a global health issue, often linked with metabolic disorders.
- Chronic sterile inflammation is a key factor in HVD, with neutrophils emerging as significant contributors.
- Neutrophils, crucial for innate immunity, are increasingly implicated in HVD pathogenesis.
Purpose of the Study:
- To review the role of inflammatory cell death signaling and neutrophil extracellular trap (NET) formation in hypertensive disease.
- To explore novel therapeutic strategies targeting NET production for cardiovascular disorders.
Main Methods:
- Literature review focusing on neutrophil function, NETosis, inflammatory cell death pathways (apoptosis, pyroptosis, necroptosis), and their involvement in HVD.
- Analysis of current research on therapeutic interventions aimed at modulating NET formation in cardiovascular disease.
Main Results:
- Neutrophil activation and NET production contribute to endothelial dysfunction, vascular remodeling, and resistance loss in HVD.
- Distinct inflammatory cell death pathways regulate NET release, influencing disease progression.
- Emerging therapies aim to inhibit NET formation, showing potential for treating cardiovascular disorders.
Conclusions:
- Inflammatory cell death and NET formation are critical mechanisms in the pathophysiology of HVD.
- Targeting NET production presents a novel therapeutic avenue for managing hypertensive vascular disease and related cardiovascular conditions.
Abstract:
Hypertensive vascular disease (HVD) is a major health burden globally and is a comorbidity commonly associated with other metabolic diseases. Many factors are associated with HVD including obesity, diabetes, smoking, chronic kidney disease, and sterile inflammation. Increasing evidence points to neutrophils as an important component of the chronic inflammatory response in HVD. Neutrophils are abundant in the circulation and can respond rapidly upon stimulation to deploy an armament of antimicrobial effector functions. One of the outcomes of neutrophil activation is the generation of neutrophil extracellular traps (NETs), a regulated extrusion of chromatin and proteases. Although neutrophils and NETs are well described as components of the innate immune response to infection, recent evidence implicates them in HVD. Endothelial cell activation can trigger neutrophil adhesion, activation, and production of NETs promoting vascular dysfunction, vessel remodelling, and loss of resistance. The regulated release of NETs can be controlled by the pore-forming activities of distinct cell death pathways. The best characterized pathways in this context are apoptosis, pyroptosis, and necroptosis. In this review, we discuss how inflammatory cell death signalling and NET formation contribute to hypertensive disease. We also examine novel therapeutic approaches to limit NET production and their future potential as therapeutic drugs for cardiovascular disorders.
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