Loss-of-function genomic variants highlight potential therapeutic targets for cardiovascular disease View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2020-12-18

AUTHORS

Jonas B. Nielsen, Oren Rom, Ida Surakka, Sarah E. Graham, Wei Zhou, Tanmoy Roychowdhury, Lars G. Fritsche, Sarah A. Gagliano Taliun, Carlo Sidore, Yuhao Liu, Maiken E. Gabrielsen, Anne Heidi Skogholt, Brooke Wolford, William Overton, Ying Zhao, Jin Chen, He Zhang, Whitney E. Hornsby, Akua Acheampong, Austen Grooms, Amanda Schaefer, Gregory J. M. Zajac, Luis Villacorta, Jifeng Zhang, Ben Brumpton, Mari Løset, Vivek Rai, Pia R. Lundegaard, Morten S. Olesen, Kent D. Taylor, Nicholette D. Palmer, Yii-Der Chen, Seung H. Choi, Steven A. Lubitz, Patrick T. Ellinor, Kathleen C. Barnes, Michelle Daya, Nicholas Rafaels, Scott T. Weiss, Jessica Lasky-Su, Russell P. Tracy, Ramachandran S. Vasan, L. Adrienne Cupples, Rasika A. Mathias, Lisa R. Yanek, Lewis C. Becker, Patricia A. Peyser, Lawrence F. Bielak, Jennifer A. Smith, Stella Aslibekyan, Bertha A. Hidalgo, Donna K. Arnett, Marguerite R. Irvin, James G. Wilson, Solomon K. Musani, Adolfo Correa, Stephen S. Rich, Xiuqing Guo, Jerome I. Rotter, Barbara A. Konkle, Jill M. Johnsen, Allison E. Ashley-Koch, Marilyn J. Telen, Vivien A. Sheehan, John Blangero, Joanne E. Curran, Juan M. Peralta, Courtney Montgomery, Wayne H-H Sheu, Ren-Hua Chung, Karen Schwander, Seyed M. Nouraie, Victor R. Gordeuk, Yingze Zhang, Charles Kooperberg, Alexander P. Reiner, Rebecca D. Jackson, Eugene R. Bleecker, Deborah A. Meyers, Xingnan Li, Sayantan Das, Ketian Yu, Jonathon LeFaive, Albert Smith, Tom Blackwell, Daniel Taliun, Sebastian Zollner, Lukas Forer, Sebastian Schoenherr, Christian Fuchsberger, Anita Pandit, Matthew Zawistowski, Sachin Kheterpal, Chad M. Brummett, Pradeep Natarajan, David Schlessinger, Seunggeun Lee, Hyun Min Kang, Francesco Cucca, Oddgeir L. Holmen, Bjørn O. Åsvold, Michael Boehnke, Sekar Kathiresan, Goncalo R. Abecasis, Y. Eugene Chen, Cristen J. Willer, Kristian Hveem

ABSTRACT

Pharmaceutical drugs targeting dyslipidemia and cardiovascular disease (CVD) may increase the risk of fatty liver disease and other metabolic disorders. To identify potential novel CVD drug targets without these adverse effects, we perform genome-wide analyses of participants in the HUNT Study in Norway (n = 69,479) to search for protein-altering variants with beneficial impact on quantitative blood traits related to cardiovascular disease, but without detrimental impact on liver function. We identify 76 (11 previously unreported) presumed causal protein-altering variants associated with one or more CVD- or liver-related blood traits. Nine of the variants are predicted to result in loss-of-function of the protein. This includes ZNF529:p.K405X, which is associated with decreased low-density-lipoprotein (LDL) cholesterol (P = 1.3 × 10−8) without being associated with liver enzymes or non-fasting blood glucose. Silencing of ZNF529 in human hepatoma cells results in upregulation of LDL receptor and increased LDL uptake in the cells. This suggests that inhibition of ZNF529 or its gene product should be prioritized as a novel candidate drug target for treating dyslipidemia and associated CVD. More... »

PAGES

6417

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  • Journal

    TITLE

    Nature Communications

    ISSUE

    1

    VOLUME

    11

    Author Affiliations

  • K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, NTNU, Trondheim, Norway
  • Department of Internal Medicine: Cardiology, University of Michigan, Ann Arbor, MI, USA
  • Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI, USA
  • Department of Biostatistics, University of Michigan School of Public Health, Ann Arbor, MI, USA
  • Center for Statistical Genetics, University of Michigan School of Public Health, Ann Arbor, MI, USA
  • Istituto di Ricerca Genetica e Biomedica, Consiglio Nazionale delle Ricerche (CNR), Monserrato, Cagliari, Italy
  • Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA
  • Department of Dermatology, St. Olav’s Hospital, Trondheim University Hospital, Trondheim, Norway
  • Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Copenhagen, Copenhagen, Denmark
  • The Institute for Translational Genomics and Population Sciences, Department of Pediatrics and Los Angeles Biomedical Research Institute, Harbor-UCLA, Torrance, CA, USA
  • Department of Biochemistry, Wake Forest School of Medicine, Winston-Salem, NC, USA
  • Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA, USA
  • Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA
  • Colorado Center for Personalized Medicine, School of Medicine, University of Colorado, Aurora, CO, USA
  • Harvard Medical School, Boston, MA, USA
  • Department of Biochemistry, Larner College of Medicine, University of Vermont, Burlington, VT, USA
  • Framingham Heart Study, Framingham, MA, USA
  • Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA
  • GeneSTAR Research Program, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA
  • Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA
  • Survey Research Center, Institute for Social Research, University of Michigan, Ann Arbor, MI, USA
  • 23andMe, Inc., Sunnyvale, CA, USA
  • The University of Alabama at Birmingham, Birmingham, AL, USA
  • Deans Office, College of Public Health, University of Kentucky, Lexington, KY, USA
  • Jackson Heart Study, Jackson, MS, USA
  • Department of Medicine, University of Mississippi Medical Center, Jackson, MS, USA
  • Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA
  • BloodWorks Northwest, University of Washington, Seattle, WA, USA
  • Department of Medicine, Duke University Medical Center, Durham, NC, USA
  • Department of Pediatrics, Division of Hematology/Oncology, Baylor College of Medicine, Houston, TX, USA
  • South Texas Diabetes and Obesity Institute, University of Texas Rio Grande Valley School of Medicine, Brownsville, TX, USA
  • Department of Genes and Human Disease, Oklahoma Medical Research Foundation, Oklahoma, OK, USA
  • Division of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan
  • Institute of Population Health Sciences, National Health Research Institutes, Miaoli, Taiwan
  • Division of Biostatistics, Washington University School of Medicine, St. Louis, MO, USA
  • University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
  • University of Illinois at Chicago, Chicago, IL, USA
  • Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA
  • Department of Epidemiology, University of Washington, Seattle, WA, USA
  • Division of Endocrinology, Diabetes and Metabolism, Ohio State University, Columbus, OH, USA
  • Division of Pharmacogenomics University of Arizona, Tucson, AR, USA
  • Division of Genetics, Genomics and Precision Medicine, Department of Medicine, University of Arizona, Tucson, AR, USA
  • Institute of Genetic Epidemiology, Department of Genetics and Pharmacology, Medical University of Innsbruck, Innsbruck, Austria
  • Institute for Biomedicine, Eurac Research, Bolzano, Italy
  • Department of Anesthesiology, University of Michigan, Ann Arbor, MI, USA
  • Center for Genomic Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
  • Laboratory of Genetics, National Institute on Aging, US National Institutes of Health, Baltimore, MD, USA
  • Dipartimento di Scienze Biomediche, Università degli Studi di Sassari, Sassari, Italy
  • HUNT Research Centre, Department of Public Health and Nursing, Norwegian University of Science and Technology, Levanger, Norway
  • Department of Endocrinology, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
  • Broad Institute, Cambridge, MD, USA
  • Regeneron Pharmaceuticals, Tarrytown, NY, USA
  • Levanger Hospital, Nord-Trøndelag Hospital Trust, Levanger, Norway
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-020-20086-3

    DOI

    http://dx.doi.org/10.1038/s41467-020-20086-3

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/33339817


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    38 schema:description Pharmaceutical drugs targeting dyslipidemia and cardiovascular disease (CVD) may increase the risk of fatty liver disease and other metabolic disorders. To identify potential novel CVD drug targets without these adverse effects, we perform genome-wide analyses of participants in the HUNT Study in Norway (n = 69,479) to search for protein-altering variants with beneficial impact on quantitative blood traits related to cardiovascular disease, but without detrimental impact on liver function. We identify 76 (11 previously unreported) presumed causal protein-altering variants associated with one or more CVD- or liver-related blood traits. Nine of the variants are predicted to result in loss-of-function of the protein. This includes ZNF529:p.K405X, which is associated with decreased low-density-lipoprotein (LDL) cholesterol (P = 1.3 × 10−8) without being associated with liver enzymes or non-fasting blood glucose. Silencing of ZNF529 in human hepatoma cells results in upregulation of LDL receptor and increased LDL uptake in the cells. This suggests that inhibition of ZNF529 or its gene product should be prioritized as a novel candidate drug target for treating dyslipidemia and associated CVD.
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