Acute myocardial infarction has long been the leading cause of death in coronary heart disease, which is characterized by irreversible cardiomyocyte death and restricted blood supply. Conventional reperfusion therapy can further aggravate myocardial injury. Stem cell therapy, especially with mesenchymal stem cells (MSCs), has emerged as a promising approach to promote cardiac repair and improve cardiac function. MSCs may induce these effects by secreting exosomes containing therapeutically active RNA, proteins and lipids. Notably, normal cardiac function depends on intracardiac paracrine signaling via exosomes, and exosomes secreted by cardiac cells can partially reflect changes in the heart during disease, so analyzing these vesicles may provide valuable insights into the pathology of myocardial infarction as well as guide the development of new treatments. The present review examines how exosomes produced by MSCs and cardiac cells may influence injury after myocardial infarction and serve as therapies against such injury.Graphical Abstract

Ischemic heart disease (IHD) is a leading cause of disability and death worldwide, with immune regulation playing a crucial role in its pathogenesis. Various immune cells are involved, and as one of the key immune cells residing in the heart, macrophages play an indispensable role in the inflammatory and reparative processes during cardiac ischemia. Exosomes, extracellular vesicles containing lipids, nucleic acids, proteins, and other bioactive molecules, have emerged as important mediators in the regulatory functions of macrophages and hold promise as a novel therapeutic target for IHD. This review summarizes the regulatory mechanisms of different subsets of macrophages and their secreted exosomes during cardiac ischemia over the past five years. It also discusses the current status of clinical research utilizing macrophages and their exosomes, as well as strategies to enhance their therapeutic efficacy through biotechnology. The aim is to provide valuable insights for the treatment of IHD.

Rationale: Temporal lobe epilepsy (TLE) is a prevalent, drug-resistant neurological disorder that causes severe disability, highlighting the need to identify novel therapeutic targets. Emerging evidence reveals widespread transcriptional dysregulation during epileptogenesis, in which multiple dysregulated genes functionally contribute to disease progression. However, the epigenetic basis of these transcriptomic changes remains poorly characterized. Methods: We established experimental epilepsy models and systematically investigated the remodeling of major histone methylation modifications during epileptogenesis using integrated low-throughput molecular assays and epigenomic profiling. Through pharmacological and genetic interventions, combined with synchronized video-EEG monitoring, whole-cell patch-clamp recordings, multi-omics analyses, and in vivo/ex vivo molecular biology approaches, we mechanistically dissected the pathological role of elevated histone H3 lysine 4 trimethylation (H3K4me3) in epileptogenesis. Results: We demonstrated the dynamic increase in H3K4me3, an epigenetic marker of transcriptional activation, during TLE development. Both pharmacological inhibition of the WD repeat-containing protein 5 (WDR5)-lysine methyltransferase 2 (KMT2) methyltransferase complex and neuron-specific WDR5 knockdown consistently conferred anti-epileptogenic effects. Mechanistically, integrated ChIP-seq and RNA-seq analyses identified AT-rich interactive domain-containing protein 5B (ARID5B) as a key WDR5-targeted effector in hippocampal neurons. WDR5 enhances H3K4me3 deposition at the Arid5b promoter to drive its transcriptional upregulation. The upregulated ARID5B protein subsequently represses γ-aminobutyric acid type A receptor (GABAAR) subunit expression, impairing inhibitory synaptic transmission and facilitating epileptogenesis. In addition, the WDR5-H3K4me3 axis may directly or indirectly regulate genes involved in glutamatergic synaptic transmission. Conclusions: The neuronal WDR5-H3K4me3 axis is an important epigenetic driver in epileptogenesis, providing both mechanistic insights and promising therapeutic targets for early intervention.

Circular RNAs (circRNAs) are covalently closed non-coding RNAs with diverse regulatory functions, high stability, and tissue specificity. This review examines their biogenesis, molecular mechanisms, experimental evidence, biomarker potential, and therapeutic implications in acute heart failure and chronic heart failure. By functioning as microRNA sponges, interacting with RNA-binding proteins, acting as protein scaffolds, undergoing cap-independent translation, and participating in stress-response signaling, circRNAs may regulate heart failure progression. Representative circRNAs, including circHIPK3, circSIRT1, circSLC8A1, circRNA-00203, and HRCR, have been linked to cardiomyocyte injury, calcium homeostasis, apoptosis, hypertrophy, fibrosis, inflammation, and ventricular remodeling. Circulating and exosome-derived circRNAs may also serve as biomarkers for diagnosis, prognosis, and disease monitoring. However, clinical translation remains limited by challenges in detection and standardization, low transcript abundance, tissue and cell heterogeneity, delivery efficiency, off-target effects, immunogenicity, and insufficient validation in large clinical cohorts. Most available evidence comes from preclinical models of myocardial infarction, pressure overload, and cardiac remodeling; evidence in heart failure with preserved ejection fraction , heart failure with mildly reduced ejection fraction, and large human populations remains limited. Overall, circRNAs provide new insights into heart failure pathophysiology and represent promising candidates for biomarker development and targeted therapy, but rigorous clinical validation is required before routine application.

Fungal infections pose a substantial threat to public health worldwide due to the ubiquitous presence of fungi in ecosystems, including soil, organic matter, and living organisms such as mammals an...