“Rather than over-relying on animal models to understand what happens in humans, isn’t it time to embrace human “model” to move forward?” The conclusion of the editorial of the Nature Medicine Editorial (April issue) screams out VPH technology is the step forward.
A recent study showing that mice do not reproduce the patterns of gene expression inducted by human inflammatory disease has provoked renewed discussions on the validity of animal models in translational research and inspired the conclusion reported in the Nature Medicine editorial.
The study outcome (J. Seok et al., “Genomic responses in mouse models poorly mimic human inflammatory diseases,” Proceedings of the National Academy of Sciences, doi/10.1073/pnas.1222878110, 2013.) details the oft-suspected limits of murine models for studying inflammatory response, and emphasizes the need for research on human physiology.
Biomedical scientists have long relied on experimentation in mice to explore human disease and evaluate drug candidates. But mouse models do not accurately reflect the genetic and proteomic responses to acute inflammatory stress in humans. In the paper it is actually demonstrated that the responses in corresponding mouse models correlate poorly with the human conditions and also, one another: the correlation of the gene changes in the mouse models with their human disease counterparts are close to those expected by random chances alone.
The study might have its caveats, but the message that mice are an imperfect model for human diseases is far from new and these recent results should be of strong motivation to continue investing on the VPH modeling technologies.
