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Updated: Mar 22, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Human Validation of Genes Associated With a Murine Atherosclerotic Phenotype
Gerard Pasterkamp1, Sander W van der Laan1, Saskia Haitjema1
1From the Laboratory of Experimental Cardiology, Division Heart and Lungs (G.P., S.W.v.d.L., S.H., M.A.S., T.B., J.v.S., I.E.H., S.C.A.d.J., H.M.d.R.), Laboratory of Clinical Chemistry and Hematology, Division Laboratories and Pharmacy (G.P.), and Division Heart and Lungs, Department of Cardiology (F.W.A.), University Medical Center Utrecht, Utrecht, The Netherlands; Vascular Biology Unit, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (H.F.A., J.L.M.B.); Institut für Schlaganfall- und Demenzforschung (ISD) Klinikum der Universität München, Munich, Germany (M.D., R.M.); Munich Cluster for Systems Neurology (SyNergy), Munich, Germany (M.D.); Department of Neurology, University of Virginia, Charlottesville (B.B.W.); Klinik für Herz- und Kreislauferkrankungen, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany (H.S.); Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V., Partner Site Munich Heart Alliance, Munich, Germany (H.S.); Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom (N.J.S.); Leicester National Institute of Health Research Biomedical Research Unit in Cardiovascular Disease, Leicester, United Kingdom (N.J.S.); Department of Surgery, National University of Singapore, Singapore (D.P.V.d.K.); Cardiovascular Research Institute (CVRI), National University Health System, Singapore, Singapore (D.P.V.d.K.); Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands (D.P.V.d.K.); Department of Neurosciences, University of Cambridge, Cambridge, United Kingdom (H.S.M.); The Roslin Institute, University of Edinburgh, Edinburgh, United Kingdom (T.M.); Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY (J.L.M.B.); Department of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estoni
Objective:
The genetically modified mouse is the most commonly used animal model for studying the pathogenesis of atherosclerotic disease. We aimed to assess if mice atherosclerosis-related genes could be validated in human disease through examination of results from genome-wide association studies.
Approach And Results:
We performed a systematic review to identify atherosclerosis-causing genes in mice and carried out gene-based association tests of their human orthologs for an association with human coronary artery disease and human large artery ischemic stroke. Moreover, we investigated the association of these genes with human atherosclerotic plaque characteristics. In addition, we assessed the presence of tissue-specific cis-acting expression quantitative trait loci for these genes in humans. Finally, using pathway analyses we show that the putative atherosclerosis-causing genes revealed few associations with human coronary artery disease, large artery ischemic stroke, or atherosclerotic plaque characteristics, despite the fact that the majority of these genes have cis-acting expression quantitative trait loci.
Conclusions:
A role for genes that has been observed in mice for atherosclerotic lesion development could scarcely be confirmed by studying associations of disease development with common human genetic variants. The value of murine atherosclerotic models for selection of therapeutic targets in human disease remains unclear.
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