Jaana A Hartiala1, James R Hilser1,2, Subarna Biswas1,3, Aldons J Lusis4,5,6, Hooman Allayee7,8. 1. Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, 2250 Alcazar Street, CSC202, Los Angeles, CA, 90033, USA. 2. Department of Biochemistry and Molecular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA. 3. Department of Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA. 4. Department of Medicine, David Geffen School of Medicine of UCLA, Los Angeles, CA, 90095, USA. 5. Department of Microbiology, David Geffen School of Medicine of UCLA, Los Angeles, CA, 90095, USA. 6. Department of Human Genetics, David Geffen School of Medicine of UCLA, Los Angeles, CA, 90095, USA. 7. Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, 2250 Alcazar Street, CSC202, Los Angeles, CA, 90033, USA. hallayee@usc.edu. 8. Department of Biochemistry and Molecular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA. hallayee@usc.edu.
Abstract
PURPOSE OF REVIEW: We provide an overview of recent findings with respect to gene-environment (GxE) interactions for cardiovascular disease (CVD) risk and discuss future opportunities for advancing the field. RECENT FINDINGS: Over the last several years, GxE interactions for CVD have mostly been identified for smoking and coronary artery disease (CAD) or related risk factors. By comparison, there is more limited evidence for GxE interactions between CVD outcomes and other exposures, such as physical activity, air pollution, diet, and sex. The establishment of large consortia and population-based cohorts, in combination with new computational tools and mouse genetics platforms, can potentially overcome some of the limitations that have hindered human GxE interaction studies and reveal additional association signals for CVD-related traits. The identification of novel GxE interactions is likely to provide a better understanding of the pathogenesis and genetic liability of CVD, with significant implications for healthy lifestyles and therapeutic strategies.
PURPOSE OF REVIEW: We provide an overview of recent findings with respect to gene-environment (GxE) interactions for cardiovascular disease (CVD) risk and discuss future opportunities for advancing the field. RECENT FINDINGS: Over the last several years, GxE interactions for CVD have mostly been identified for smoking and coronary artery disease (CAD) or related risk factors. By comparison, there is more limited evidence for GxE interactions between CVD outcomes and other exposures, such as physical activity, air pollution, diet, and sex. The establishment of large consortia and population-based cohorts, in combination with new computational tools and mouse genetics platforms, can potentially overcome some of the limitations that have hindered human GxE interaction studies and reveal additional association signals for CVD-related traits. The identification of novel GxE interactions is likely to provide a better understanding of the pathogenesis and genetic liability of CVD, with significant implications for healthy lifestyles and therapeutic strategies.
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