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.

Silicosis is an incurable chronic disease characterized by lung fibrosis and inflammation. The combination of tetrandrine and Buyang Huanwu Decoction (BYHWD) has a curative effect on silicosis. However, the mechanism of action and the key active constituent in BYHWD are still unclear. The present study employed network pharmacology and molecular docking to determine the mechanism of action and the key active components of BYHWD of Tetrandrine in combination with BYHWD for silicosis. The primary elements and targets of BYHWD were obtained from the Traditional Chinese Medicine Systems Pharmacology and analysis platform. The targets associated with tetrandrine and silicosis were identified and extracted from the Comparative Toxicogenomics Database and GeneCards database. The potential targets for the treatment of silicosis using a combination of Tetrandrine and BYHWD were identified by considering the overlapping targets between compound drugs and silicosis. These targets were then utilized to construct protein-protein interaction networks, compound drug-ingredient-target networks, and perform enrichment analyses. The top 5 active ingredients present in the compound drug-ingredient-target network are tetrandrine, quercetin, luteolin, kaempferol, and beta-carotene. Similarly, the top 6 hub genes in the protein-protein interaction network are FGF2, MMP-9, MMP-1, IL-10, IL-17A, and IL-6. The molecular docking suggested that the active components may easily access the active pocket of the hub gene. The in-silico investigation suggested that quercetin might be the active component in BYHWD responsible for therapeutic effectiveness against silicosis. This study identified the active compound and potential molecular mechanism underlying the therapeutic effects of BYHWD in combination with tetrandrine for treating silicosis. Notably, we found that quercetin may serve as the key compound in BYHWD for the treatment of silicosis.

Introduction: The effectiveness of thromboelastography (TEG)-guided antiplatelet therapy in patients with ischemic cerebrocardiovascular diseases is not well-established. This systematic review evaluates the efficacy and safety of TEG-guided antiplatelet therapy compared to standard treatment in patients with ischemic cerebrocardiovascular diseases. Methods: Randomized controlled trials (RCTs) and observational studies comparing TEG-guided antiplatelet therapy with standard therapy in patients suffering from ischemic stroke (IS) or coronary artery disease (CAD) were identified. The primary efficacy measure was a composite of ischemic and hemorrhagic events. Secondary efficacy measures included any ischemic events, while safety was assessed by the occurrence of bleeding events. Results: Ten studies involving 4 RCTs and 6 observational studies with a total of 1,678 patients were included. When considering a composite of ischemic and hemorrhagic events in RCTs, a significant reduction was observed in IS or CAD patients under TEG-guided therapy compared to standard therapy (OR: 0.45, 95% CI: 0.27–0.75, p = 0.002). After pooling RCTs and observational studies together, compared to standard antiplatelet therapy, TEG-guided therapy significantly reduced the risk of a composite of ischemic and hemorrhagic events (OR: 0.26, 95% CI: 0.19–0.37; p < 0.00001), ischemic events (OR: 0.28, 95% CI: 0.19–0.41; p < 0.00001), and bleeding events (OR: 0.31, 95% CI: 0.16–0.62; p = 0.0009) in patients with IS or CAD. Conclusion: TEG-guided antiplatelet therapy appears to be both effective and safe for patients with IS or CAD. These findings support the use of TEG testing to tailor antiplatelet therapy in individuals with ischemic cerebrocardiovascular diseases.