The BMAL1/HIF2A heterodimer modulates circadian variations of myocardial injury.

ABSTRACT: Acute myocardial infarction stands as a prominent cause of morbidity and mortality worldwide^1-6. Clinical studies have demonstrated that the severity of cardiac injury following myocardial infarction exhibits a circadian pattern, with larger infarct sizes and poorer outcomes in patients experiencing morning onset myocardial infarctions^7-14. However, the molecular mechanisms that govern circadian variations of myocardial injury remain unclear. Here, we show that BMAL1^14-20, a core circadian transcription factor, orchestrates diurnal variability in myocardial injury. Unexpectedly, BMAL1 modulates circadian-dependent cardiac injury by forming a transcriptionally active heterodimer with a non-canonical partner, hypoxia-inducible factor 2 alpha (HIF2A)^6,21-

SUBMITTER: Ruan W 

PROVIDER: S-EPMC10925443 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature