Genomic responses in mouse models greatly mimic human inflammatory diseases

TLDR

Mice have long been essential in biomedical research, yet a recent report questioned their relevance by claiming mouse genomic responses poorly mimic human inflammatory diseases. The authors reanalyzed the same gene expression datasets, focusing on genes significantly altered in both species, and performed a meta‑analysis that identified pathways and biogroups commonly regulated across multiple human and mouse inflammatory conditions. The reanalysis revealed strong correlations between mouse and human gene expression (Spearman 0.43–0.68, 77–93% concordant direction, P = 6.5 × 10⁻¹¹ to 1.2 × 10⁻³⁵), showing that mouse models closely recapitulate human inflammatory gene expression and supporting their continued use.

Abstract

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.