PDF(Pubmed)
Abstract：
The role of the extracellular matrix (ECM) in Parkinson\'s disease (PD) is not well understood, even though it is critical for neuronal structure and signaling. This systematic review identified the top deregulated ECM-related pathways in studies that used gene set enrichment analyses (GSEA) to document transcriptomic, proteomic, or genomic alterations in PD. PubMed and Google scholar were searched for transcriptomics, proteomics, or genomics studies that employed GSEA on data from PD tissues or cells and reported ECM-related pathways among the top-10 most enriched versus controls. Twenty-seven studies were included, two of which used multiple omics analyses. Transcriptomics and proteomics studies were conducted on a variety of tissue and cell types. Of the 17 transcriptomics studies (16 data sets), 13 identified one or more adhesion pathways in the top-10 deregulated gene sets or pathways, primarily related to cell adhesion and focal adhesion. Among the 8 proteomics studies, 5 identified altered overarching ECM gene sets or pathways among the top 10. Among the 4 genomics studies, 3 identified focal adhesion pathways among the top 10. The findings summarized here suggest that ECM organization/structure and cell adhesion (particularly focal adhesion) are altered in PD and should be the focus of future studies.
摘要：
细胞外基质（ECM）在帕金森病（PD）中的作用尚不清楚，尽管它对神经元结构和信号传导至关重要。本系统综述在使用基因集富集分析（GSEA）记录转录组学的研究中确定了顶级的ECM相关通路，蛋白质组学，或PD的基因组改变。搜索PubMed和谷歌学者的转录组学，蛋白质组学，或基因组学研究采用GSEA对PD组织或细胞的数据进行研究，并报道了前10名富集度最高的对照中的ECM相关途径。包括27项研究，其中两个使用了多个组学分析。对多种组织和细胞类型进行转录组学和蛋白质组学研究。在17项转录组学研究(16个数据集)中，13鉴定了前10个失调的基因集或途径中的一个或多个粘附途径，主要与细胞粘附和局灶性粘附有关。在8项蛋白质组学研究中,5在前10名中鉴定了改变的总体ECM基因集或途径。在4项基因组学研究中，3在前10名中确定了粘着斑途径。本文总结的研究结果表明，ECM组织/结构和细胞粘附（特别是局灶性粘附）在PD中发生了变化，应成为未来研究的重点。
