One of the ways in which the immune cells known as neutrophils attack pathogens is to release structures called neutrophil extracellular traps into the intracellular environment. These traps can disable pathogens, but like much of the activity of the immune system, too much of a good thing becomes harmful. Excessive neutrophil generation of traps in the aged tissue environment promotes chronic inflammation, and here researchers focus specific on the consequences of this activity in the vasculature, where it promotes the onset of cardiovascular disease. While relatively little work has been carried out on approaches to clear traps or reduce the pace of their creation, a range of evidence suggests that this might be a viable strategy to improve the state of the aged vasculature.
Blood vessels are critical in systemic aging with arteries stiffening and calcifying due to chronic inflammation and oxidative stress, driving age-related cardiovascular and cerebrovascular diseases. In this review, neutrophil extracellular traps (NETs) – web-like structures composed of decondensed chromatin, histones, and antimicrobial proteins released by neutrophils – are explored as therapeutic targets in vascular aging.
NETs are vital for pathogen defense, but their excessive activation leads to inflammation and vascular pathologies, promoting endothelial dysfunction, inflammatory aging, and vascular remodeling in diseases such as hypertension, atherosclerosis, myocardial infarction, heart failure, atrial fibrillation, ischemic stroke, and Alzheimer’s disease. Increasing evidence supports that modulating NETs through inhibitors or scavengers can reduce inflammatory responses, preserve endothelial integrity, and improve prognosis. As a potential therapeutic target, growing attention has been directed toward exploring the balance between NET induction, inhibition, and degradation.
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