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Abstract：
Methylation is a biochemical process involving the addition of a methyl group (-CH3) to various chemical compounds. It plays a crucial role in maintaining the homeostasis of the endothelium, which lines the interior surface of blood vessels, and has been linked, among other conditions, to coronary artery disease (CAD). Despite significant progress in CAD diagnosis and treatment, intensive research continues into genotypic and phenotypic CAD biomarkers. This review explores the significance of the methylation pathway and folate metabolism in CAD pathogenesis, with a focus on endothelial dysfunction resulting from deficiency in the active form of folate (5-MTHF). We discuss emerging areas of research into CAD biomarkers and factors influencing the methylation process. By highlighting genetically determined methylation disorders, particularly the MTHFR polymorphism, we propose the potential use of the active form of folate (5-MTHF) as a novel CAD biomarker and personalized pharmaceutical for selected patient groups. Our aim is to improve the identification of individuals at high risk of CAD and enhance their prognosis.
摘要：
甲基化是涉及向各种化学化合物添加甲基(-CH3)的生化过程。它在维持内皮的稳态中起着至关重要的作用，排列在血管的内表面，并且已经联系在一起，除其他条件外，冠状动脉疾病（CAD）。尽管在CAD诊断和治疗方面取得了重大进展，对基因型和表型CAD生物标志物的深入研究仍在继续。本文就甲基化通路和叶酸代谢在CAD发病机制中的意义作一综述。重点是由于缺乏活性形式的叶酸（5-MTHF）而导致的内皮功能障碍。我们讨论了CAD生物标志物和影响甲基化过程的因素的新兴研究领域。通过强调基因决定的甲基化障碍，特别是MTHFR多态性，我们建议将活性形式的叶酸(5-MTHF)作为一种新的CAD生物标志物和针对特定患者组的个性化药物。我们的目标是提高对冠心病高危个体的识别并改善其预后。
