■勃起功能障碍(ED)与抑郁症之间的临床相关性已在累积研究中得到揭示。然而,它们之间共享机制的证据不足。本研究旨在探讨与ED和抑郁症相关的常见转录组改变。
■从基因表达综合(GEO)数据库收集与ED和抑郁相关的基因集。进行比较分析以获得常见基因。使用R软件和其他适当的工具,我们进行了一系列的分析,包括功能富集,交互式网络创建,基因簇分析,以及转录和转录后特征谱分析。经过外部验证和分子实验,选择了ED和抑郁症之间的候选枢纽交联。此外,研究了hub基因的亚群位置和疾病关联。
■在ED和抑郁症之间总共鉴定出85个共同基因。这些基因与细胞粘附密切相关,氧化还原稳态,活性氧代谢过程,和神经元细胞体。由此开发了由80种蛋白质和216种相互作用组成的相互作用网络。对常见基因的蛋白质组签名的分析突出了八个主要的共享基因:CLDN5,COL7A1,LDHA,MAP2K2,RETSAT,SEMA3A,TAGLN,TBC1D1。这些基因参与血管形态发生和肌肉细胞活性。随后的转录因子(TF)-miRNA网络显示与共享基因相关的47个TFs和88个miRNA。最后,CLDN5和TBC1D1已得到很好的验证,并被确定为ED和抑郁症之间的中心交联。这些基因在海绵体和脑组织中具有特定的亚群位置,分别。
■我们的研究首次探讨了常见的转录组改变以及ED和抑郁症的共同生物学作用。这项研究的发现提供了对抑郁症和ED共存的参考分子机制的见解。
UNASSIGNED: The clinical correlation between erectile dysfunction (ED) and depression has been revealed in cumulative studies. However, the evidence of shared mechanisms between them was insufficient. This study aimed to explore common transcriptomic alterations associated with ED and depression.
UNASSIGNED: The gene sets associated with ED and depression were collected from the Gene Expression Omnibus (GEO) database. Comparative analysis was conducted to obtain common genes. Using R software and other appropriate tools, we conducted a range of analyses, including function enrichment, interactive network creation, gene cluster analysis, and transcriptional and post-transcriptional signature profiling. Candidate hub crosslinks between ED and depression were selected after external validation and molecular experiments. Furthermore, subpopulation location and disease association of hub genes were explored.
UNASSIGNED: A total of 85 common genes were identified between ED and depression. These genes strongly correlate with cell adhesion, redox homeostasis, reactive oxygen species metabolic process, and neuronal cell body. An interactive network consisting of 80 proteins and 216 interactions was thereby developed. Analysis of the proteomic signature of common genes highlighted eight major shared genes: CLDN5, COL7A1, LDHA, MAP2K2, RETSAT, SEMA3A, TAGLN, and TBC1D1. These genes were involved in blood vessel morphogenesis and muscle cell activity. A subsequent transcription factor (TF)-miRNA network showed 47 TFs and 88 miRNAs relevant to shared genes. Finally, CLDN5 and TBC1D1 were well-validated and identified as the hub crosslinks between ED and depression. These genes had specific subpopulation locations in the corpus cavernosum and brain tissue, respectively.
UNASSIGNED: Our study is the first to investigate common transcriptomic alterations and the shared biological roles of ED and depression. The findings of this study provide insights into the referential molecular mechanisms underlying the co-existence between depression and ED.