TY - JOUR
AU - Junhee Seok
AU - H. Shaw Warren
AU - Alex G. Cuenca
AU - Michael N. Mindrinos
AU - Henry V. Baker
AU - Weihong Xu
AU - Daniel R. Richards
AU - Grace P. McDonald-Smith
AU - Hong Gao
AU - Laura Hennessy
AU - Celeste C. Finnerty
AU - Cecilia M. López
AU - Shari Honari
AU - Ernest E. Moore
AU - Joseph P. Minei
AU - Joseph Cuschieri
AU - Paul E. Bankey
AU - Jeffrey L. Johnson
AU - Jason Sperry
AU - Avery B. Nathens
AU - Timothy R. Billiar
AU - Michael A. West
AU - Marc G. Jeschke
AU - Matthew B. Klein
AU - Richard L. Gamelli
AU - Nicole S. Gibran
AU - Bernard H. Brownstein
AU - Carol Miller-Graziano
AU - Steve E. Calvano
AU - Philip H. Mason
AU - J. Perren Cobb
AU - Laurence G. Rahme
AU - Stephen F. Lowry
AU - Ronald V. Maier
AU - Lyle L. Moldawer
AU - David N. Herndon
AU - Ronald W. Davis
AU - Wenzhong Xiao
AU - Ronald G. Tompkins
AU - the Inflammation and Host Response to Injury, Large Scale Collaborative Research Program
AU - Amer Abouhamze
AU - Ulysses G. J. Balis
AU - David G. Camp
AU - Asit K. De
AU - Brian G. Harbrecht
AU - Douglas L. Hayden
AU - Amit Kaushal
AU - Grant E. O’Keefe
AU - Kenneth T. Kotz
AU - Weijun Qian
AU - David A. Schoenfeld
AU - Michael B. Shapiro
AU - Geoffrey M. Silver
AU - Richard D. Smith
AU - John D. Storey
AU - Robert Tibshirani
AU - Mehmet Toner
AU - Julie Wilhelmy
AU - Bram Wispelwey
AU - Wing H Wong
AB - A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry new drug candidates forward into clinical trials. Systematic studies evaluating how well murine models mimic human inflammatory diseases are nonexistent. Here, we show that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another. Among genes changed significantly in humans, the murine orthologs are close to random in matching their human counterparts (e.g., R2 between 0.0 and 0.1). In addition to improvements in the current animal model systems, our study supports higher priority for translational medical research to focus on the more complex human conditions rather than relying on mouse models to study human inflammatory diseases.
BT - Proceedings of the National Academy of Sciences
DA - 2013-02-26
DO - 10.1073/pnas.1222878110
IS - 9
N2 - A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry new drug candidates forward into clinical trials. Systematic studies evaluating how well murine models mimic human inflammatory diseases are nonexistent. Here, we show that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another. Among genes changed significantly in humans, the murine orthologs are close to random in matching their human counterparts (e.g., R2 between 0.0 and 0.1). In addition to improvements in the current animal model systems, our study supports higher priority for translational medical research to focus on the more complex human conditions rather than relying on mouse models to study human inflammatory diseases.
PY - 2013
SP - 3507
EP - 3512
T2 - Proceedings of the National Academy of Sciences
TI - Genomic responses in mouse models poorly mimic human inflammatory diseases
UR - https://www.pnas.org/doi/10.1073/pnas.1222878110
VL - 110
Y2 - 2022-12-01
ER -