Department of Biological Sciences, North Carolina State University, Raleigh, North Carolina 27695, USA.
Center for Human Health and the Environment, North Carolina State University, Raleigh, North Carolina 27695, USA.
Toxicol Sci. 2023 Sep 28;195(2):155-168. doi: 10.1093/toxsci/kfad069.
The molecular mechanisms connecting environmental exposures to adverse endpoints are often unknown, reflecting knowledge gaps. At the Comparative Toxicogenomics Database (CTD), we developed a bioinformatics approach that integrates manually curated, literature-based interactions from CTD to generate a "CGPD-tetramer": a 4-unit block of information organized as a step-wise molecular mechanism linking an initiating Chemical, an interacting Gene, a Phenotype, and a Disease outcome. Here, we describe a novel, user-friendly tool called CTD Tetramers that generates these evidence-based CGPD-tetramers for any curated chemical, gene, phenotype, or disease of interest. Tetramers offer potential solutions for the unknown underlying mechanisms and intermediary phenotypes connecting a chemical exposure to a disease. Additionally, multiple tetramers can be assembled to construct detailed modes-of-action for chemical-induced disease pathways. As well, tetramers can help inform environmental influences on adverse outcome pathways (AOPs). We demonstrate the tool's utility with relevant use cases for a variety of environmental chemicals (eg, perfluoroalkyl substances, bisphenol A), phenotypes (eg, apoptosis, spermatogenesis, inflammatory response), and diseases (eg, asthma, obesity, male infertility). Finally, we map AOP adverse outcome terms to corresponding CTD terms, allowing users to query for tetramers that can help augment AOP pathways with additional stressors, genes, and phenotypes, as well as formulate potential AOP disease networks (eg, liver cirrhosis and prostate cancer). This novel tool, as part of the complete suite of tools offered at CTD, provides users with computational datasets and their supporting evidence to potentially fill exposure knowledge gaps and develop testable hypotheses about environmental health.
将环境暴露与不良结局联系起来的分子机制通常是未知的,这反映了知识上的差距。在比较毒理学基因组学数据库(CTD)中,我们开发了一种生物信息学方法,该方法整合了来自 CTD 的人工策展、基于文献的相互作用,以生成“CGPD-四聚体”:一个 4 个单位的信息块,组织为一个逐步的分子机制,将起始化学物质、相互作用的基因、表型和疾病结果联系起来。在这里,我们描述了一种名为 CTD Tetramers 的新颖、用户友好的工具,它可以为任何经过策展的化学物质、基因、表型或疾病生成这些基于证据的 CGPD-四聚体。四聚体为连接化学物质暴露与疾病的未知潜在机制和中间表型提供了潜在的解决方案。此外,还可以组装多个四聚体来构建化学诱导疾病途径的详细作用模式。同样,四聚体可以帮助告知环境对不良结局途径(AOPs)的影响。我们通过各种环境化学物质(例如全氟烷基物质、双酚 A)、表型(例如细胞凋亡、精子发生、炎症反应)和疾病(例如哮喘、肥胖、男性不育)的相关用例展示了该工具的实用性。最后,我们将 AOP 不良结局术语映射到相应的 CTD 术语,允许用户查询可以帮助用其他胁迫物、基因和表型来增强 AOP 途径的四聚体,并制定潜在的 AOP 疾病网络(例如,肝硬化和前列腺癌)。作为 CTD 提供的全套工具的一部分,这个新工具为用户提供了计算数据集及其支持证据,以潜在地填补暴露知识空白,并制定有关环境健康的可测试假设。