Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
December 8, 2025Blood

Hematopoietic JAK2V617F mutation increases susceptibility to atrial fibrillation via NLRP3 inflammasome activation in macrophages

View Full Paper
Ask AI
Bookmark
Share

Authors

GTGuangshuai TengKSKe ShangCDChenxiao Du

Discussion

Loading...

Member takes

Overview

Retrospective analysis reveals JAK2V617F mutation links to increased atrial fibrillation risk in myeloid malignancies, suggesting inflammatory pathways as a target for ruxolitinib treatment.

Key Points

  • JAK2V617F mutation increases atrial fibrillation risk, revealing a direct causal relationship with macrophage activation.
  • Co-culture studies demonstrated JAK2VFBMDMs promoted fibrosis-related protein expression in atrial fibroblasts, indicated by key cytokines.
  • Retrospective analysis showed JAK2V617F mutation as an independent risk factor for new-onset atrial fibrillation with HR of 2.20 (95% CI: 1.45-3.35).
  • Ruxolitinib treatment significantly lowered incidence of new-onset atrial fibrillation in JAK2V617F-mutant patients, emphasizing inflammation's role.

Cite This Study

Teng et al. (2025) studied this question.

synapsesocial.com/papers/69362f3a4fa91c937236d443https://doi.org/10.1182/blood-2025-634
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Abstract Fri066: Role of Inflammation and JAK/STAT3 Signaling in AML Mediated Atrial Fibrillation2025
  2. 2Germline Jak2-R1063H mutation interferes with normal hematopoietic development and increases risk of thrombosis and leukemic transformation2025 · 3 citations
  3. 3HiJAKing the Hematopoietic System: A Low-Frequency JAK2V617F Clone Drives Myeloproliferative Neoplasm Pathology2025 · 3 citations
  4. 4Clonal Hematopoiesis of Intermediate Potential in Atrial Fibrillation: A Critical View of Current Knowledge as a Springboard for Future Research2025 · 1 citations
  5. 5The anti-MPL antibody AMM2 prevents cardiovascular dysfunction in a mouse model of myeloproliferative neoplasms2025