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Sepsis is a systemic inflammatory response triggered by infection, which can result in multiple organ dysfunctions, including disseminated intravascular coagulation (DIC) and acute lung injury (ALI), ultimately leading to patient mortality. The pathophysiology of sepsis is intricate, involving excessive immune activation, cytokine storms, endothelial damage, and microcirculatory dysfunction. Dysregulated host responses frequently give rise to severe complications, markedly elevating mortality rates. Neutrophil extracellular traps (NETs) are web-like structures consisting of DNA, histones, and granular proteins, released by neutrophils upon activation. Ongoing research into NETs has uncovered their significant pathophysiological roles in clinical conditions, including sepsis. This review outlines the mechanisms of NET formation, release, classification, detection methods, and relevant biomarkers. Additionally, it delves into the signaling pathways involved in NET generation, their pathophysiological implications in sepsis and its complications, and evaluates their potential utility in clinical laboratory diagnostics.
Yan et al. (Sat,) studied this question.