Abstract
Translation modifications, particularly those involving histone deacetylases (HDACs), are crucial for regulating gene expression and have significant implications for cardiovascular disease (CVD). The association between HDACs and CVD has garnered significant research interest due to the pivotal role of HDACs in gene expression regulation and cellular function. Aberrant HDAC activity has been implicated in various pathological processes underlying CVD, including inflammation, endothelial dysfunction, hypertrophy, fibrosis, and atherosclerosis. This review explores the molecular mechanisms by which different HDAC isoforms influence cardiovascular pathology, highlighting evidence from preclinical and clinical studies. Emerging data suggest that HDAC inhibitors could offer therapeutic potential by modulating these processes and improving cardiovascular health. However, the precise isoform-specific roles and therapeutic window for HDAC inhibition in CVD remain to be elucidated. Furthermore, research is essential to identify the crucial and complex relationship between HDACs and cardiovascular health, which could pave the way for novel, targeted interventions for the treatment of CVD.