Recent studies have found a link between deep vein thrombosis and inflammatory reactions. N6-methyladenosine (m6A), a crucial element in immunological regulation, is believed to contribute to the pathophysiology of venous thromboembolism (VTE). However, how the m6A-modified immune microenvironment is involved in VTE remains unclear. In the present study, we identified a relationship between VTE and the expression of several m6A regulatory elements by analyzing peripheral blood samples from 177 patients with VTE and 88 healthy controls from public GEO databases GSE19151 and GSE48000. We used machine learning to identify essential genes and constructed a diagnostic model for VTE using multivariate logistic regression. Unsupervised cluster analysis revealed a marked difference between m6A modification patterns in terms of immune cell infiltration, inflammatory reactivity, and autophagy. We identified two m6A-related autophagy genes (i.e., CHMP2B and SIRT1) and the crucial m6A regulator YTHDF3 using bioinformatics. We also examined two potential mechanisms through which YTHDF3 may affect VTE. m6A modification, immunity, and autophagy are closely linked in VTE, offering novel mechanistic and therapeutic insights. • The identification of a relationship between VTE and the expression of m6A regulatory elements through analysis of patient samples, highlighting the role of m6A methylation in VTE pathophysiology. • The development of a diagnostic model using machine learning techniques to predict VTE occurrence, demonstrating the potential for improved early diagnosis and treatment strategies. • Findings that altered m6A methylation patterns influence immune cell infiltration, inflammatory reactivity, and autophagy in VTE, suggesting new therapeutic targets. • The identification of key m6A-related autophagy genes and their mechanisms, providing insights into the complex interactions between RNA methylation, immune response, and autophagy in VTE. • Implications of the study for the development of innovative therapeutics for VTE, emphasizing the potential of targeting m6A regulatory factors and their mediated mechanisms.

中文翻译：

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静脉血栓栓塞中 N6-甲基腺苷 (m6A) 调节因子介导的 RNA 甲基化模式、免疫特征和自噬相关机制

最近的研究发现深静脉血栓形成和炎症反应之间存在联系。 N6-甲基腺苷 (m6A) 是免疫调节的关键元素，被认为与静脉血栓栓塞 (VTE) 的病理生理学有关。然而，m6A 修饰的免疫微环境如何参与 VTE 仍不清楚。在本研究中，我们通过分析来自公共 GEO 数据库 GSE19151 和 GSE48000 的 177 名 VTE 患者和 88 名健康对照者的外周血样本，确定了 VTE 与几种 m6A 调节元件表达之间的关系。我们使用机器学习来识别必需基因，并使用多元逻辑回归构建了 VTE 诊断模型。无监督聚类分析揭示了 m6A 修饰模式在免疫细胞浸润、炎症反应性和自噬方面存在显着差异。我们利用生物信息学鉴定了两个 m6A 相关自噬基因（即 CHMP2B 和 SIRT1）和关键的 m6A 调节因子 YTHDF3。我们还研究了 YTHDF3 可能影响 VTE 的两种潜在机制。 m6A 修饰、免疫和自噬在 VTE 中密切相关，提供了新颖的机制和治疗见解。 • 通过分析患者样本确定VTE 与m6A 调节元件表达之间的关系，强调m6A 甲基化在VTE 病理生理学中的作用。 • 使用机器学习技术开发诊断模型来预测 VTE 的发生，展示了改进早期诊断和治疗策略的潜力。 • m6A 甲基化模式改变影响 VTE 中免疫细胞浸润、炎症反应性和自噬的研究结果，提出了新的治疗靶点。 • 鉴定关键的m6A 相关自噬基因及其机制，深入了解VTE 中RNA 甲基化、免疫反应和自噬之间的复杂相互作用。 • 该研究对开发 VTE 创新疗法的意义，强调了针对 m6A 调节因子及其介导机制的潜力。