DNA-sensing inflammasomes cause recurrent atherosclerotic stroke.

ABSTRACT: The risk of early recurrent events after stroke remains high despite currently established secondary prevention strategies¹. Risk is particularly high in patients with atherosclerosis, with more than 10% of patients experiencing early recurrent events^1,2. However, despite the enormous medical burden of this clinical phenomenon, the underlying mechanisms leading to increased vascular risk and recurrent stroke are largely unknown. Here, using a novel mouse model of stroke-induced recurrent ischaemia, we show that stroke leads to activation of the AIM2 inflammasome in vulnerable atherosclerotic plaques via an increase of circulating cell-free DNA. Enhanced plaque inflammation post-stroke results in plaque destabilization and atherothrombosis, finally leading to arterioar

SUBMITTER: Cao J 

PROVIDER: S-EPMC11390481 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature