Myocardial infarction augments sleep to limit cardiac inflammation and damage.

ABSTRACT: Sleep is integral to cardiovascular health^1,2. Yet, the circuits that connect cardiovascular pathology and sleep are incompletely understood. It remains unclear whether cardiac injury influences sleep and whether sleep-mediated neural outputs contribute to heart healing and inflammation. Here we report that in humans and mice, monocytes are actively recruited to the brain after myocardial infarction (MI) to augment sleep, which suppresses sympathetic outflow to the heart, limiting inflammation and promoting healing. After MI, microglia rapidly recruit circulating monocytes to the brain's thalamic lateral posterior nucleus (LPN) via the choroid plexus, where they are reprogrammed to generate tumour necrosis factor (TNF). In the thalamic LPN, monocytic TNF engages Tnfrsf1a-express

SUBMITTER: Huynh P 

PROVIDER: S-EPMC11998484 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature