Int J Biol Macromol. 2026 Aug 9:154006. doi: 10.1016/j.ijbiomac.2026.154006. Online ahead of print.
ABSTRACT
Cardiovascular diseases (CVDs) remain a leading cause of morbidity and mortality worldwide, yet the epigenetic mechanisms that connect stress signals to durable transcriptional remodeling are incompletely understood. The BRG1/BRM-associated factor (BAF) chromatin remodeling complexes, mammalian members of the SWItch/sucrose non-fermentable (SWI/SNF) family, regulate chromatin accessibility by repositioning nucleosomes and by cooperating with transcription factors and histone-modifying enzymes. Recent structural and functional studies classify mammalian BAF complexes into three major subtypes including canonical BAF (cBAF), polybromo-associated BAF (PBAF), and non-canonical BAF (ncBAF), with distinct subunit compositions and disease-relevant genomic targeting. In this review, we synthesize evidence linking BAF-dependent chromatin remodeling to myocardial infarction, ischemia-reperfusion injury, heart failure, diabetic cardiomyopathy, cardiac hypertrophy, arrhythmia, congenital heart disease, atherosclerosis, and aortic aneurysm. We emphasize subtype and subunit specific mechanisms, including inflammatory signaling, oxidative stress responses, fetal gene reactivation, ion-channel transcription, extracellular-matrix remodeling, and post-translational regulation of BAF-associated proteins. Finally, we discuss tissue-specific delivery, context-dependent effects, and the need to target disease-relevant protein-protein interfaces, providing potentially new theoretical basis and potential research directions for the prevention and treatment of CVD.
PMID:42571864 | DOI:10.1016/j.ijbiomac.2026.154006