Ontology highlight
ABSTRACT: Background –
The Jak2 V617F (Jak2 VF ) mutation is an important cause of both clonal hematopoiesis of indeterminate potential (CHIP) and myeloproliferative neoplasms (MPN). Mouse models of Jak2 VF CHIP and MPN show accelerated atherosclerosis progression, driven by macrophage inflammasome activation. We undertook the present study to assess the hypothesis that ongoing inflammation would impede atherosclerosis resolution in Jak2 VF mice.Methods and results –
Chimeric Jak2 VF/WT or control WT/WT bone marrow was transplanted into Ldlr -/- mice and, following 13-16 weeks of Western diet-induced atherosclerosis progression, cholest
SUBMITTER: Hardaway BD
PROVIDER: S-EPMC12324260 | biostudies-literature | 2025 Nov
REPOSITORIES: biostudies-literature