Abstract
Thrombosis leads to ischemic organ damage in cardiovascular and thromboembolic diseases.
Neutrophils promote thrombosis in vitro and in vivo by releasing neutrophil extracellular
traps (NETs). NETs are composed of DNA filaments coated with histones and neutrophil
enzymes such as myeloperoxidase (MPO). Circulating extracellular DNA (ceDNA) is widely
used as a surrogate marker to monitor NET formation in thrombosis. This narrative
review summarizes the association of ceDNA with human thrombosis. Levels of ceDNA
indicate the extent and outcome of several cardiovascular and thromboembolic diseases,
including myocardial infarction, stroke, and venous thromboembolism. ceDNA correlates
with markers of coagulation and platelet consumption, thus supporting the hypothesis
that ceDNA may be a surrogate marker of thrombus formation. In addition, ceDNA levels
correlate with markers of cell injury and size of ischemic lesions, suggesting that
ceDNA does not derive from NETs but is probably released from damaged organs. Few
studies identified NET-specific biomarkers such as DNA–MPO complexes in the blood
of patients with thrombosis. In conclusion, it remains to be established whether ceDNA
in patients derives from NETs and is a cause or consequence of thrombosis.
Keywords
thrombosis - biomarker - extracellular DNA - cell-free DNA - plasma DNA - neutrophil
extracellular traps