Neutrophil Extracellular Traps: Signaling Properties and Disease Relevance

Table 3

List of studies showing association between NETs and atherosclerosis.

Authors, reference	Study design	Main study findings
Warnatsch et al. [8]	Using a mouse model	Cholesterol crystals triggered neutrophils to release NETs. NETs primed macrophages for cytokine production in atherosclerosis and blocking NETs formation significantly attenuated the plaque progression.
Liu et al. [86]	Using a mouse model	NETs are present in atherosclerotic lesions and are associated with the development of atherosclerosis. Specific deletion of PAD4 in the myeloid lineage diminished NET formation and significantly reduced atherosclerosis burden.
Knight et al. [87]	Using a mouse model	Pharmacological interventions that block NET formation via targeting PAD4 can reduce atherosclerosis burden and arterial thrombosis
Franck et al. [88]	Using a mouse model	NETs do not influence chronic experimental atherogenesis, but participate causally in acute thrombotic complications of intimal lesions that recapitulate features of superficial erosion.
Quillard et al. [93]	Analyzing 56 specimens of human carotid plaques.	NETs are present in human atherosclerotic plaques and associate with the number of luminal apoptotic ECs.
Pertiwi et al. [94]	Analyzing 12 thrombosed plaques obtained at autopsy from patients with acute MI.	NETs dominate numerically in early thrombosis and macrophage traps in late (organizing) thrombosis.
Stakos et al. [62]	Cell experiments (neutrophils obtained from patients with STEMI)	Neutrophils isolated from blood samples obtained by IRA have a higher ability to form NETs compared with those isolated from blood samples obtained by non-IRA.

NET: neutrophil extracellular traps; PAD4: peptidylarginine deiminase 4; ECs: endothelial cells; MI: myocardial infarction; STEMI: ST-elevation myocardial infarction; IRA: infarct-related coronary arteries.