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Circulating Extracellular DNA: Cause or Consequence of Thrombosis?
Miguel Jiménez-Alcázar1, Natalie Kim1, Tobias A Fuchs1
1Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Seminars in Thrombosis and Hemostasis
|March 31, 2017
Summary
Circulating extracellular DNA (ceDNA) is linked to thrombosis and ischemic organ damage. While ceDNA may indicate disease severity, its origin from neutrophil extracellular traps (NETs) or damaged organs in thrombosis requires further investigation.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Immunology
Background:
- Thrombosis causes ischemic organ damage in cardiovascular and thromboembolic diseases.
- Neutrophils release neutrophil extracellular traps (NETs), which promote thrombosis.
- Circulating extracellular DNA (ceDNA) is used as a marker for NET formation in thrombosis.
Purpose of the Study:
- To review the association between ceDNA and human thrombosis.
- To evaluate ceDNA as a surrogate marker for thrombus formation and disease outcomes.
Main Methods:
- Narrative review of existing literature.
- Analysis of correlations between ceDNA levels and clinical outcomes, coagulation markers, and markers of cell injury.
Main Results:
- ceDNA levels correlate with the extent and outcomes of myocardial infarction, stroke, and venous thromboembolism.
- ceDNA correlates with markers of coagulation and platelet consumption.
- ceDNA levels also correlate with markers of cell injury and ischemic lesion size, suggesting organ damage as a potential source.
Conclusions:
- ceDNA may serve as a surrogate marker for thrombosis severity and outcomes.
- The origin of ceDNA in thrombosis (NETs vs. organ damage) is not definitively established.
- Further research is needed to clarify the role of ceDNA in thrombosis and its relationship with NETs.