Genomic responses in mouse models greatly mimic human inflammatory diseases 论文

2014Proceedings of the National Academy of Sciences引用 510
Cytokine Signaling Pathways and InteractionsComputational Drug Discovery MethodsAnimal testing and alternatives

详细信息

发表期刊/会议
Proceedings of the National Academy of Sciences
发表日期
2014-08-04
发表年份
2014

关键词

Cytokine Signaling Pathways and InteractionsComputational Drug Discovery MethodsAnimal testing and alternatives

摘要

The use of mice as animal models has long been considered essential in modern biomedical research, but the role of mouse models in research was challenged by a recent report that genomic responses in mouse models poorly mimic human inflammatory diseases. Here we reevaluated the same gene expression datasets used in the previous study by focusing on genes whose expression levels were significantly changed in both humans and mice. Contrary to the previous findings, the gene expression levels in the mouse models showed extraordinarily significant correlations with those of the human conditions (Spearman's rank correlation coefficient: 0.43-0.68; genes changed in the same direction: 77-93%; P = 6.5 × 10(-11) to 1.2 × 10(-35)). Moreover, meta-analysis of those datasets revealed a number of pathways/biogroups commonly regulated by multiple conditions in humans and mice. These findings demonstrate that gene expression patterns in mouse models closely recapitulate those in human inflammatory conditions and strongly argue for the utility of mice as animal models of human disorders.

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