Cardiovascular disease (CVD) stands as the foremost cause of patient mortality, and the lack of early diagnosis and defined treatment targets significantly contributes to the suboptimal prevention and management of CVD. Myocardial fibrosis (MF) is not only a complex pathogenic process with no effective treatment currently available but also exerts detrimental effects on the progression of various cardiovascular diseases, thereby escalating their mortality rates. Exosomes are nanoscale biocommunication vehicles that facilitate intercellular communication by transporting bioactive substances, such as nucleic acids and proteins, from specific cell types. Numerous studies have firmly established that microRNAs (miRNAs), as non-coding RNAs, wield post-transcriptional regulatory mechanisms and exhibit close associations with various CVDs, including coronary heart disease (CHD), atrial fibrillation (AF), and heart failure (HF). MiRNAs hold significant promise in the diagnosis and treatment of cardiovascular diseases. In this review, we provide a concise introduction to the biological attributes of exosomes and exosomal miRNAs. We also explore the roles and mechanisms of distinct cell-derived exosomal miRNAs in the context of myocardial fibrosis. These findings underscore the pivotal role of exosomes in the diagnosis and treatment of cardiac fibrosis and emphasize their potential as biotherapies and drug delivery vectors for cardiac fibrosis treatment.

Fraxin is a bioactive compound derived from Cortex Fraxini. It is known for its diverse biological activities and numerous benefits, including anti-inflammatory, antioxidant, analgesic, antimicrobial, antiviral, and immunomodulatory effects. Despite growing interest in natural compounds for cardiovascular diseases Fraxin’s atheroprotective properties and molecular targets have not yet been fully elucidated. To address this gap, our research employed an integrated approach combining network pharmacology, molecular docking simulations, and in vitro biological validation to systematically unravel Fraxin’s therapeutic mechanisms against atherosclerosis (AS). The results showed that 84 potential targets for Fraxin against AS were predicted through public databases, and the key target TLR4 was identified by protein–protein interaction and molecular docking analysis. GO enrichment and KEGG pathway analysis revealed that these potential targets were significantly enriched in the PI3K-Akt and oxidative stress responses pathways. Subsequently conducted in vitro studies validated that Fraxin modulates the TLR4/PI3K/Akt signaling pathway to suppress reactive oxygen species generation and downregulate pro-inflammatory cytokines including Il1b, Il6, and Tnf thereby slowing atherosclerotic disease advancement. This investigation methodically delineates Fraxin’s therapeutic targets and underlying molecular mechanisms in AS management, establishing a scientific foundation for its potential translation into clinical practice.