Atrial fibrillation (AF) is a complex disease and affects millions of people around the world. The biological mechanisms that are involved with AF are complex and still need to be fully elucidated. Therefore, we performed a meta-analysis of transcriptome data related to AF to explore these mechanisms aiming at more sensitive and reliable results. Public transcriptomic datasets were downloaded, analyzed for quality control, and individually pre-processed. Differential expression analysis was carried out for each individual dataset, and the results were meta-analytically aggregated using the r-th ordered p-value method. We analyzed the final list of differentially expressed genes through network analysis, namely topological and modularity analysis, and functional enrichment analysis. The meta-analysis of transcriptomes resulted in 589 differentially expressed genes, whose protein-protein interaction network presented 11 hubs-bottlenecks and four main identified functional modules. These modules were enriched for, respectively, 23, 54, 33, and 53 biological pathways involved with the pathophysiology of AF, especially with the disease's structural and electrical remodeling processes. Stress of the endoplasmic reticulum, protein catabolism, oxidative stress, and inflammation are some of the enriched processes. Among hubs-bottlenecks genes, which are highly connected and probably have a key role in regulating these processes, we found HSPA5, ANK2, CTNNB1, and VWF. Further experimental investigation of our findings may shed light on the pathophysiology of the disease and contribute to the identification of new therapeutic targets and treatments.

中文翻译：

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转录组数据的荟萃分析揭示了房颤相关的病理生理模块。

心房颤动（AF）是一种复杂的疾病，影响着全球数百万人。与房颤有关的生物学机制很复杂，仍然需要充分阐明。因此，我们对与AF相关的转录组数据进行了荟萃分析，以探索这些机制，旨在获得更加敏感和可靠的结果。下载公共转录组数据集，进行质量控制分析，并进行单独预处理。对每个单独的数据集进行差异表达分析，并使用第r个有序p值方法对结果进行荟萃分析汇总。我们通过网络分析，即拓扑和模块性分析以及功能富集分析，分析了差异表达基因的最终清单。转录组的荟萃分析产生了589个差异表达的基因，其蛋白质-蛋白质相互作用网络显示了11个枢纽，瓶颈和四个主要鉴定的功能模块。这些模块分别丰富了23种，54种，33种和53种与房颤的病理生理学有关的生物学途径，尤其是与疾病的结构和电重构过程有关的生物学途径。内质网的应激，蛋白质分解代谢，氧化应激和炎症是一些富集过程。在高度紧密联系并且可能在调节这些过程中起关键作用的枢纽瓶颈基因中，我们发现了HSPA5，ANK2，CTNNB1和VWF。