Ticagrelor, acting as a reversible platelet aggregation inhibitor of P2Y12 receptors (P2Y12R), is regarded as one of the first-line antiplatelet drugs for acute cardiovascular diseases. Though the probability of ticagrelor resistance is much lower than that of clopidogrel, there have been recent reports of ticagrelor resistance. In this review, we summarized the clinical application of ticagrelor and then presented the criteria and current status of ticagrelor resistance. We further discussed the potential mechanisms for ticagrelor resistance in terms of drug absorption, metabolism, and receptor action. In conclusion, the incidences of ticagrelor resistance fluctuated between 0 and 20%, and possible mechanisms mainly arose from its absorption and receptor action. Specifically, a variety of factors, such as the drug form of ticagrelor, gut microecology, and the expression and function of P-glycoprotein (P-gp) and P2Y12R, have been shown to be associated with ticagrelor resistance. The exact mechanisms of ticagrelor resistance warrant further exploration, which may contribute to the diagnosis and treatment of ticagrelor resistance.

N⁶-methyladenosine (m⁶A) modification is a newly discovered regulatory mechanism in eukaryotes. As one of the most common epigenetic mechanisms, m⁶A’s role in the development of atherosclerosis (AS) and atherosclerotic diseases (AD) has also received increasing attention. Herein, we elucidate the effect of m⁶A on major risk factors for AS, including lipid metabolism disorders, hypertension, and hyperglycemia. We also describe how m⁶A methylation contributes to endothelial cell injury, macrophage response, inflammation, and smooth muscle cell response in AS and AD. Subsequently, we illustrate the m⁶A-mediated aberrant biological role in the pathogenesis of AS and AD, and analyze the levels of m⁶A methylation in peripheral blood or local tissues of AS and AD, which helps to further discuss the diagnostic and therapeutic potential of m⁶A regulation for AS and AD. In summary, studies on m⁶A methylation provide new insights into the pathophysiologic mechanisms of AS and AD, and m⁶A methylation could be a novel diagnostic biomarker and therapeutic target for AS and AD.

The high incidence and mortality rates of cardiovascular and cerebrovascular diseases make them a significant global health challenge. Antiplatelet drugs play a central role in the prevention and treatment of these diseases. Despite the wide range of available antiplatelet drugs, antiplatelet drug resistance is not rare. So optimizing drug use through personalized treatment strategies to achieve maximum therapeutic benefit remains a major challenge in clinical practice. Non-coding RNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), have made significant progress in understanding their regulatory roles in drug resistance, becoming a frontier area of current research. In addition to the regulatory functions of non-coding RNAs, emerging studies have highlighted the role of RNA modifications, such as N6-methyladenosine (m6A), in the regulation of gene expression and cellular processes involved in antiplatelet drug resistance. These modifications contribute to the stability, splicing, and translation of RNA, further influencing their roles in drug resistance mechanisms. In recent years, significant progress has been made in the research of non-coding RNAs and RNA modifications, revealing their crucial roles in the mechanisms of antiplatelet drug resistance. This review focuses on the latest advancements in non-coding RNA research related to antiplatelet drug resistance and explores the emerging field of RNA modifications. It analyzes potential underlying mechanisms and discusses future research directions, aiming to provide new theoretical support and research perspectives for personalized precision antiplatelet.

Ischemic stroke (IS) is characterized by a high incidence rate, high disability rate and high recurrence rate. The existing treatment methods have limitations such as a narrow time window and limited recovery of neurological function. Bone marrow mesenchymal stem cells (BMSCs) have become a research hotspot in the regenerative treatment of IS due to their multi-directional differentiation potential, paracrine regulation and immune regulation characteristics. This review explores the mechanism of action, strategies for enhancing therapeutic efficacy and the progress of clinical transformation of BMSCs in the treatment of IS. Basic research indicates that BMSCs improve neurological function through multiple mechanisms such as migrating to ischemic foci, secreting neurotrophic factors, promoting angiogenesis, and inhibiting apoptosis of nerve cells. Gene modification technology and the application of exosomes can further potentiate therapeutic efficacy. The optimization of injection routes, cell types, transplantation time Windows and cell doses is crucial to the therapeutic effect. Clinical studies have initially confirmed the safety of BMSCs treatment and some functional improvement effects, but there are still problems such as small sample size and unclear long-term efficacy. In the future, it is necessary to further clarify the treatment mechanism, optimize the treatment plan, and promote the transformation of basic research into clinical practice (Graphical Abstract).