■流行病学研究表明,脂质代谢紊乱与发展动脉硬化(AS)和腹主动脉瘤(AAA)的风险增加之间存在联系。然而,脂代谢之间的精确关系,AS,AAA仍然没有被完全理解。这项研究的目的是检查AS和AAA之间共享的途径和潜在的脂肪酸代谢相关基因(FRG)。
■AS和AAA相关数据集从基因表达综合(GEO)数据库中检索,和limma包用于鉴定AS和AAA患者常见的差异表达FRGs(DFRGs)。对(DFRGs)进行了功能富集分析,建立了蛋白质-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)进行特征基因的选择。随后,使用筛选过程的结果绘制了列线图,关键基因在两个独立的外部数据集(GSE28829和GSE17901)以及临床样本中进行了验证。最后,单样本基因组富集分析(ssGSEA)用于评估AS和AAA的免疫细胞模式。此外,评价关键串扰基因与免疫细胞的相关性。
■与对照组相比,AS和AAA患者的脂肪酸代谢评分均降低.我们在AS和AAA中发现40个DFRG重叠,脂质和氨基酸代谢在其发病机理中至关重要。PCBD1,ACADL,MGLL,BCKDHB,和IDH3G被鉴定为连接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品中得到证实。免疫浸润分析显示,中性粒细胞,NKCD56dim细胞,和Tem细胞在AS和AAA发展中起重要作用。相关分析表明,这些特征基因可能与免疫细胞浸润有关。
■脂肪酸代谢途径似乎与AS和AAA的发展有关。此外,PCBD1,ACADL,MGLL,BCKDHB,和IDH3G有可能作为AS并发AAA患者的诊断标志物。
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.