Inflammasome Signaling, Thromboinflammation, and Venous Thromboembolism

© 2023 The Authors..

Venous thromboembolism (VTE) remains a major health burden despite anticoagulation advances, suggesting incomplete management of pathogenic mechanisms. The NLRP3 (NACHT-, LRR- and pyrin domain-containing protein 3) inflammasome, interleukin (IL)-1, and pyroptosis are emerging contributors to the inflammatory pathogenesis of VTE. Inflammasome pathway activation occurs in patients with VTE. In preclinical models, inflammasome signaling blockade reduces venous thrombogenesis and vascular injury, suggesting that this therapeutic approach may potentially maximize anticoagulation benefits, protecting from VTE occurrence, recurrence, and ensuing post-thrombotic syndrome. The nonselective NLRP3 inhibitor colchicine and the anti-IL-1β agent canakinumab reduce atherothrombosis without increasing bleeding. Rosuvastatin reduces primary venous thrombotic events at least in part through lipid-lowering independent mechanisms, paving the way to targeted anti-inflammatory strategies in VTE. This review outlines recent preclinical and clinical evidence supporting a role for inflammasome pathway activation in venous thrombosis, and discusses the, yet unexplored, therapeutic potential of modulating inflammasome signaling to prevent and manage VTE.

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:8

Enthalten in:

JACC. Basic to translational science - 8(2023), 9 vom: 03. Sept., Seite 1245-1261

Sprache:

Englisch

Beteiligte Personen:

Potere, Nicola [VerfasserIn]
Abbate, Antonio [VerfasserIn]
Kanthi, Yogendra [VerfasserIn]
Carrier, Marc [VerfasserIn]
Toldo, Stefano [VerfasserIn]
Porreca, Ettore [VerfasserIn]
Di Nisio, Marcello [VerfasserIn]

Links:

Volltext

Themen:

Anti-inflammatory agents
Blood coagulation
Embolism and thrombosis
Inflammation
Interleukin-1
Journal Article
Post-thrombotic syndrome
Review

Anmerkungen:

Date Revised 05.03.2024

published: Electronic-eCollection

Citation Status PubMed-not-MEDLINE

doi:

10.1016/j.jacbts.2023.03.017

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM362850585