The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis.

ABSTRACT: Clonal haematopoiesis, which is highly prevalent in older individuals, arises from somatic mutations that endow a proliferative advantage to haematopoietic cells. Clonal haematopoiesis increases the risk of myocardial infarction and stroke independently of traditional risk factors¹. Among the common genetic variants that give rise to clonal haematopoiesis, the JAK2^V617F (JAK2^VF) mutation, which increases JAK-STAT signalling, occurs at a younger age and imparts the strongest risk of premature coronary heart disease^1,2. Here we show increased proliferation of macrophages and prominent formation of necrotic cores in atherosclerotic lesions in mice that express Jak2^VF selectively in macrophages, and in chimeric mice that model clonal haema

SUBMITTER: Fidler TP 

PROVIDER: S-EPMC8038646 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature