Research Progress on Mechanisms of JAK2 Mutations in Coagulation Factor Regulation and Thrombosis
10.3971/j.issn.1000-8578.2026.26.0005
- VernacularTitle:JAK2突变在凝血因子调控与血栓形成中的机制研究进展
- Author:
Hongning LI
1
;
Huimin ZHU
2
;
Yuan DU
1
;
Jinjin ZHANG
3
;
Zhiyong CHENG
3
Author Information
1. Department of Laboratory, Baoding Hospital, Guang'anmen Hospital, Baoding 071000, China.
2. Graduate School, Hebei North University, Zhangjiakou 075000, China;Department of Hematology, Baoding No. 1 Hospital, Baoding 071000, China.
3. Department of Hematology, Baoding No. 1 Hospital, Baoding 071000, China.
- Publication Type:REVIEWS
- Keywords:
JAK2 V617F;
Thrombosis;
JAK-STAT pathway;
Myeloproliferative neoplasms
- From:
Cancer Research on Prevention and Treatment
2026;53(8):642-650
- CountryChina
- Language:Chinese
-
Abstract:
The JAK2 V617F mutation is a key molecular event in myeloproliferative neoplasms and is strongly associated with an increased risk of thrombosis. This review aims to summarize the underlying mechanisms, clinical manifestations, and management strategies for thrombosis driven by the JAK2 V617F mutation. Relevant recent studies are analyzed to evaluate the effect of the mutation on molecular signaling, hematopoietic cell function, inflammatory activation, endothelial injury, and coagulation imbalance. Findings indicate that the JAK2 V617F mutation induces the persistent activation of the JAK-STAT pathway, leading to erythroid clonal expansion, platelet hyperreactivity, and enhanced neutrophil chemotaxis, along with excessive inflammatory cytokine release, NET formation, and platelet-leukocyte aggregation. These processes collectively promote endothelial dysfunction and hypercoagulation, ultimately contributing to arterial and venous thrombosis. Clinically, affected patients may present with coronary artery events deep vein thrombosis, and portal vein thrombosis, often accompanied by high recurrence rates and poor outcomes. In conclusion, the JAK2 V617F mutation drives thrombosis via multiple intertwined mechanisms, suggesting that future therapeutic strategies should integrate anticoagulation, anti-inflammation therapy, NET inhibition, and targeted JAK-STAT pathway blockade to improve patient survival.
