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Neutrophil extracellular traps mediate neuro-immunothrombosis

Neural Regen Res, 2024 · DOI: https://doi.org/10.4103/1673-5374.389625 · Published: August 1, 2024

Cardiovascular ScienceImmunology

Simple Explanation

Neutrophil extracellular traps (NETs) are released by neutrophils and are composed of DNA and histones. They promote inflammation and thrombosis when stimulated by inflammatory reactions. Neuro-immunothrombosis summarizes the interplay between inflammation and thrombosis during neural development and the pathogenesis of neurological diseases. NETs play a crucial role in immunothrombosis, and identified modulators of neuro-immunothrombosis. This review discusses the role of neutrophil extracellular traps in neuro-immunothrombosis and explores potential therapeutic interventions.

Study Duration
Not specified
Participants
Not specified
Evidence Level
Review

Key Findings

  • 1
    NETs are key mediators of inflammation and thrombosis, and have been widely accepted as a mechanism of deep vein thrombosis.
  • 2
    BBB destruction disrupts the balance between hemostasis and clotting in the CNS; BBB dysfunction after traumatic brain injury drives thrombosis and inflammation.
  • 3
    Neutrophil elastase degrades the BBB, causing secondary CNS damage in ischemic stroke that identifies the neuroinflammatory mechanisms associated with NETs.

Research Summary

Neutrophil extracellular traps are primarily composed of DNA and histones and are released by neutrophils to promote inflammation and thrombosis when stimulated by various inflammatory reactions. Neuroinflammation and thrombosis in the CNS are closely associated with NETosis. The discovery of NETs has opened new avenues for understanding the principles of inflammation and thrombosis.

Practical Implications

Therapeutic Target

Inhibition of NETosis is a promising therapeutic option for thrombosis treatment.

Drug development

PAD4 inhibitors are potential drug targets for deep vein thrombosis and represent a highly attractive strategy for preventing immunothrombosis.

Clinical Intervention

Targeting NETs with DNase I may affect thrombus stability in the treatment of acute ischemic stroke, and thrombolysis in patients is more successful in vitro with DNase I added to standard tissue plasminogen activator.

Study Limitations

  • 1
    Further research is needed to understand how neutrophil extracellular traps promote blood-brain barrier disruption and immunothrombosis.
  • 2
    More research is needed to determine the possible link between antibiotics, NETs, and thrombosis.
  • 3
    Further research is needed on the role of NETs and their clinical applications in TBI.

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