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Platelet Jak2 deficiency accelerates atherosclerosis with increased inflammatory response.


ABSTRACT: Cardiovascular disease (CVD) is the leading cause of mortality worldwide, of which atherosclerosis is the major pathology. Chronic inflammation underlies atherosclerosis, and Janus kinase 2 (Jak2) is a critical signaling node that mediates this process. Jak2V617F activating mutation has recently been implicated in clonal hematopoiesis of indeterminate potential as an emerging major CVD risk factor. While platelets' role in hemostasis and thrombosis is well-established in CVD, the essential role of platelet Jak2 in mediating inflammation in atherosclerosis is unknown. To this end, we assessed the in vivo role of platelet Jak2 in atherosclerosis using ApoE-/- mice with platelet Jak2 deficiency. These mice developed accelerated atherosclerosis in the aortic roots and arc

SUBMITTER: Kim D 

PROVIDER: S-EPMC12624798 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature