Research progress on neutrophil extracellular traps in sepsis‑induced coagulopathy (Review)

Sepsis affects an estimated 166 million individuals globally with 21.4 million annual deaths and represents a notable public health challenge. Sepsis‑induced coagulopathy (SIC) is a marked complication of sepsis, characterized by dysregulated hemostasis and microvascular thrombosis. Neutrophil extracellular traps (NETs) are pivotal mediators linking innate immunity to thrombo‑inflammation in this process. The present review systematically examined the epidemiology and pathogenesis of SIC, the molecular mechanisms of NET release (suicidal, vital, mitochondrial and non‑canonical pathways) and the mechanistic pathways by which NETs regulate SIC. NETs disrupt endothelial integrity, amplify platelet activation, propagate coagulation cascades and suppress fibrinolysis, thereby establishing a self‑amplifying cycle that accelerates progression to disseminated intravascular coagulation and multiple organ failure. Furthermore, the present review highlighted current therapeutic strategies targeting NETs, including inhibition of NET synthesis, acceleration of NET clearance and disruption of platelet‑neutrophil interactions. Elucidating the central role of NETs in SIC pathophysiology may facilitate the development of novel biomarkers and precision therapeutic interventions for this life‑threatening condition.