Background:Epidemiological research has demonstrated that there is a connection between lipid metabolism disorder and an increased risk of developing arteriosclerosis (AS) and abdominal aortic aneurysm (AAA). However, the precise relationship between lipid metabolism, AS, and AAA is still not fully understood. The objective of this study was to examine the pathways and potential fatty acid metabolism-related genes (FRGs) that are shared between AS and AAA.Methods:AS- and AAA-associated datasets were retrieved from the Gene Expression Omnibus (GEO) database, and the limma package was utilized to identify differentially expressed FRGs (DFRGs) common to both AS and AAA patients. Functional enrichment analysis was conducted on the (DFRGs), and a protein-protein interaction (PPI) network was established. The selection of signature genes was performed through the utilization of least absolute shrinkage and selection operator (LASSO) regression and random forest (RF). Subsequently, a nomogram was developed using the results of the screening process, and the crucial genes were validated in two separate external datasets (GSE28829 and GSE17901) as well as clinical samples. In the end, single-sample gene set enrichment analysis (ssGSEA) was utilized to assess the immune cell patterns in both AS and AAA. Additionally, the correlation between key crosstalk genes and immune cell was evaluated.Results:In comparison to control group, both AS and AAA patients exhibited a decrease in fatty acid metabolism score. We found 40 DFRGs overlapping in AS and AAA, with lipid and amino acid metabolism critical in their pathogenesis. PCBD1, ACADL, MGLL, BCKDHB, and IDH3G were identified as signature genes connecting AS and AAA. Their expression levels were confirmed in validation datasets and clinical samples. The analysis of immune infiltration showed that neutrophils, NK CD56dim cells, and Tem cells are important in AS and AAA development. Correlation analysis suggested that these signature genes may be involved in immune cell infiltration.Conclusion:The fatty acid metabolism pathway appears to be linked to the development of both AS and AAA. Furthermore, PCBD1, ACADL, MGLL, BCKDHB, and IDH3G have the potential to serve as diagnostic markers for patients with AS complicated by AAA.

中文翻译：

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基于脂肪酸代谢基因集的转录组分析识别动脉粥样硬化和腹主动脉瘤之间的共享诊断生物标志物和免疫关系

背景：流行病学研究表明，脂质代谢紊乱与动脉硬化（AS）和腹主动脉瘤（AAA）风险增加之间存在联系。然而，脂质代谢、AS 和 AAA 之间的确切关系仍不完全清楚。本研究的目的是检查 AS 和 AAA 之间共享的途径和潜在的脂肪酸代谢相关基因 (FRG)。方法：从基因表达综合 (GEO) 数据库中检索 AS 和 AAA 相关数据集， limma 包用于识别 AS 和 AAA 患者常见的差异表达 FRG (DFRG)。对（DFRGs）进行功能富集分析，并建立蛋白质-蛋白质相互作用（PPI）网络。通过利用最小绝对收缩和选择算子（LASSO）回归和随机森林（RF）来选择特征基因。随后，使用筛选过程的结果开发了列线图，并在两个独立的外部数据集（GSE28829 和 GSE17901）以及临床样本中验证了关键基因。最后，利用单样本基因集富集分析 (ssGSEA) 来评估 AS 和 AAA 中的免疫细胞模式。此外，还评估了关键串扰基因与免疫细胞之间的相关性。结果：与对照组相比，AS和AAA患者的脂肪酸代谢评分均有所下降。我们发现 40 个 DFRG 在 AS 和 AAA 中重叠，脂质和氨基酸代谢在其发病机制中至关重要。 PCBD1、ACADL、MGLL、BCKDHB 和 IDH3G 被确定为连接 AS 和 AAA 的特征基因。它们的表达水平在验证数据集和临床样本中得到证实。免疫浸润分析表明，中性粒细胞、NK CD56dim 细胞和 Tem 细胞在 AS 和 AAA 的发生过程中发挥着重要作用。相关分析表明这些特征基因可能参与免疫细胞浸润。结论：脂肪酸代谢途径似乎与AS和AAA的发生有关。此外，PCBD1、ACADL、MGLL、BCKDHB 和 IDH3G 有潜力作为 AS 并发 AAA 患者的诊断标志物。