Cholesterol homeostasis plays a significant role in cardiovascular disease. Previous studies have indicated that ATP-binding cassette transporter A1 (ABCA1) is one of the most important proteins that maintains cholesterol homeostasis. ABCA1 mediates nascent high-density lipoprotein biogenesis. Upon binding with apolipoprotein A-I, ABCA1 facilitates the efflux of excess intracellular cholesterol and phospholipids and controls the rate-limiting step of reverse cholesterol transport. In addition, ABCA1 interacts with the apolipoprotein receptor and suppresses inflammation through a series of signaling pathways. Thus, ABCA1 may prevent cardiovascular disease by inhibiting inflammation and maintaining lipid homeostasis. Several studies have indicated that post-transcriptional modifications play a critical role in the regulation of ABCA1 transportation and plasma membrane localization, which affects its biological function. Meanwhile, carriers of the loss-of-function ABCA1 gene are often accompanied by decreased expression of ABCA1 and an increased risk of cardiovascular diseases. We summarized the ABCA1 transcription regulation mechanism, mutations, post-translational modifications, and their roles in the development of dyslipidemia, atherosclerosis, ischemia/reperfusion, myocardial infarction, and coronary heart disease.

The APOA1/C3/A4/A5 cluster is an essential component in regulating lipoprotein metabolism and maintaining plasma lipid homeostasis. A genome-wide association analysis and Mendelian randomization have revealed potential associations between genetic variants within this cluster and lipid metabolism disorders, including hyperlipidemia and cardiovascular events. An enhanced understanding of the complexity of gene regulation has led to growing recognition regarding the role of epigenetic variation in modulating APOA1/C3/A4/A5 gene expression. Intensive research into the epigenetic regulatory patterns of the APOA1/C3/A4/A5 cluster will help increase our understanding of the pathogenesis of lipid metabolism disorders and facilitate the development of new therapeutic approaches. This review discusses the biology of how the APOA1/C3/A4/A5 cluster affects circulating lipoproteins and the current progress in the epigenetic regulation of the APOA1/C3/A4/A5 cluster.

• Palmitoylation regulates protein stability, localization, and signal transduction in key pathophysiological processes. • Palmitoylation affects metabolism, inflammation, and tumorigenesis in diseases. • Palmitoylation modulates related proteins and signal transduction in the progression of cardiovascular diseases. • Targeting protein palmitoylation offers novel therapeutic potential for cardiovascular diseases.

Cardiovascular diseases (CVDs) are a leading cause of death worldwide, and new therapeutic strategies are urgently needed. In recent years, enhancer RNAs (eRNAs) have gradually attracted attention because they offer new directions for the treatment of CVDs. Super-enhancer RNAs (seRNAs) are a subset of non-coding RNAs that are transcribed from regions of the genome known as super enhancers, which are large clusters of enhancers with a high density of transcription factors and cofactors. These regions play a pivotal role in regulating genes involved in cell identity and disease progression. This article reviews the characteristics of seRNAs, their expression patterns, and regulatory mechanisms in the cardiovascular system. We also explore their role in the occurrence and development of CVDs, as well as their potential as diagnostic biomarkers and therapeutic targets. Currently, therapies targeting seRNAs are a research hotspot. The development of specific inhibitors or activators is expected to facilitate precise interventions for CVDs. In addition, the use of gene editing techniques to modify relevant eRNA introduces new possibilities for disease treatment. This review aims to provide a comprehensive overview of seRNAs in CVDs and discusses their potential as a novel class of therapeutic targets.

Cardiovascular diseases (CVDs) are a leading cause of death worldwide. In recent years, enhancer RNAs (eRNAs) have gradually attracted attention because they offer new directions for the treatment of CVDs. This article reviews the characteristics of super-enhancer RNAs (seRNAs) and their expression and regulatory mechanisms in the cardiovascular system. We also explore their role in the occurrence and development of CVDs, as well as their potential as diagnostic markers and treatment targets. Currently, therapies targeting seRNAs are a research hotspot. The development of specific inhibitors or activators is expected to facilitate precise interventions for CVDs. In addition, the use of gene editing techniques to modify relevant eRNA introduce new possibilities for disease treatment.