HDL and atherosclerotic cardiovascular disease: genetic insights into complex biology.
Identifieur interne : 000B16 ( Main/Exploration ); précédent : 000B15; suivant : 000B17HDL and atherosclerotic cardiovascular disease: genetic insights into complex biology.
Auteurs : Robert S. Rosenson [États-Unis] ; H Bryan Brewer [États-Unis] ; Philip J. Barter [Australie] ; Johan L M. Björkegren [États-Unis] ; M John Chapman [France] ; Daniel Gaudet [Canada] ; Daniel Seung Kim [États-Unis] ; Eric Niesor [Suisse] ; Kerry-Anne Rye [Australie] ; Frank M. Sacks [États-Unis] ; Jean-Claude Tardif [Canada] ; Robert A. Hegele [Canada]Source :
- Nature reviews. Cardiology [ 1759-5010 ] ; 2017.
Abstract
Plasma levels of HDL cholesterol (HDL-C) predict the risk of cardiovascular disease at the epidemiological level, but a direct causal role for HDL in cardiovascular disease remains controversial. Studies in animal models and humans with rare monogenic disorders link only particular HDL-associated mechanisms with causality, including those mechanisms related to particle functionality rather than cholesterol content. Mendelian randomization studies indicate that most genetic variants that affect a range of pathways that increase plasma HDL-C levels are not usually associated with reduced risk of cardiovascular disease, with some exceptions, such as cholesteryl ester transfer protein variants. Furthermore, only a fraction of HDL-C variation has been explained by known loci from genome-wide association studies (GWAS), suggesting the existence of additional pathways and targets. Systems genetics can enhance our understanding of the spectrum of HDL pathways, particularly those pathways that involve new and non-obvious GWAS loci. Bioinformatic approaches can also define new molecular interactions inferred from both large-scale genotypic data and RNA sequencing data to reveal biologically meaningful gene modules and networks governing HDL metabolism with direct relevance to disease end points. Targeting these newly recognized causal networks might inform the development of novel therapeutic strategies to reduce the risk of cardiovascular disease.
DOI: 10.1038/nrcardio.2017.115
PubMed: 28795686
Affiliations:
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Rosenson</name><affiliation wicri:level="1"><nlm:affiliation>Cardiometabolics Unit, Icahn School of Medicine at Mount Sinai, Hospital Box 1030, One Gustave L. Levy Place, New York, New York 10029, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiometabolics Unit, Icahn School of Medicine at Mount Sinai, Hospital Box 1030, One Gustave L. 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Barter</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Sciences, Faculty of Medicine, Level 4E, Wallace Wurth Building, University of New South Wales Sydney, 18 High Street, Sydney, Kensington New South Wales 2052, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Sciences, Faculty of Medicine, Level 4E, Wallace Wurth Building, University of New South Wales Sydney, 18 High Street, Sydney, Kensington New South Wales 2052</wicri:regionArea><wicri:noRegion>Kensington New South Wales 2052</wicri:noRegion></affiliation></author><author><name sortKey="Bjorkegren, Johan L M" sort="Bjorkegren, Johan L M" uniqKey="Bjorkegren J" first="Johan L M" last="Björkegren">Johan L M. Björkegren</name><affiliation wicri:level="1"><nlm:affiliation>Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, New York 10029, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, New York 10029</wicri:regionArea><wicri:noRegion>New York 10029</wicri:noRegion></affiliation></author><author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M John" last="Chapman">M John Chapman</name><affiliation wicri:level="1"><nlm:affiliation>National Institute for Health and Medical Research (INSERM) and Endocrinology Metabolism Service, Pitie-Salpetriere University Hospital, 83 Boulevard de l'Hôpital, 75651 Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>National Institute for Health and Medical Research (INSERM) and Endocrinology Metabolism Service, Pitie-Salpetriere University Hospital, 83 Boulevard de l'Hôpital, 75651 Paris</wicri:regionArea><wicri:noRegion>75651 Paris</wicri:noRegion><placeName><settlement type="city">Paris</settlement><region type="région" nuts="2">Île-de-France</region></placeName></affiliation></author><author><name sortKey="Gaudet, Daniel" sort="Gaudet, Daniel" uniqKey="Gaudet D" first="Daniel" last="Gaudet">Daniel Gaudet</name><affiliation wicri:level="1"><nlm:affiliation>Lipidology Unit, Community Genomic Medicine Centre and ECOGENE-21, Department of Medicine, Université de Montréal, 930 Jacques-Cartier, Saguenay, Québec G7H 7K9, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Lipidology Unit, Community Genomic Medicine Centre and ECOGENE-21, Department of Medicine, Université de Montréal, 930 Jacques-Cartier, Saguenay, Québec G7H 7K9</wicri:regionArea><wicri:noRegion>Québec G7H 7K9</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Daniel Seung" sort="Kim, Daniel Seung" uniqKey="Kim D" first="Daniel Seung" last="Kim">Daniel Seung Kim</name><affiliation wicri:level="1"><nlm:affiliation>University of Michigan School of Public Health, M4045 SPH II, 1415 Washington Heights, Ann Arbor, Michigan 48109-2029, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>University of Michigan School of Public Health, M4045 SPH II, 1415 Washington Heights, Ann Arbor, Michigan 48109-2029</wicri:regionArea><wicri:noRegion>Michigan 48109-2029</wicri:noRegion></affiliation></author><author><name sortKey="Niesor, Eric" sort="Niesor, Eric" uniqKey="Niesor E" first="Eric" last="Niesor">Eric Niesor</name><affiliation wicri:level="1"><nlm:affiliation>Hartis-Pharma Sàrl, 13c Chemin de Bonmont, 1260 Nyon, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Hartis-Pharma Sàrl, 13c Chemin de Bonmont, 1260 Nyon</wicri:regionArea><wicri:noRegion>1260 Nyon</wicri:noRegion></affiliation></author><author><name sortKey="Rye, Kerry Anne" sort="Rye, Kerry Anne" uniqKey="Rye K" first="Kerry-Anne" last="Rye">Kerry-Anne Rye</name><affiliation wicri:level="1"><nlm:affiliation>School of Medical Sciences, Faculty of Medicine, Level 4E, Wallace Wurth Building, University of New South Wales Sydney, 18 High Street, Sydney, Kensington New South Wales 2052, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Medical Sciences, Faculty of Medicine, Level 4E, Wallace Wurth Building, University of New South Wales Sydney, 18 High Street, Sydney, Kensington New South Wales 2052</wicri:regionArea><wicri:noRegion>Kensington New South Wales 2052</wicri:noRegion></affiliation></author><author><name sortKey="Sacks, Frank M" sort="Sacks, Frank M" uniqKey="Sacks F" first="Frank M" last="Sacks">Frank M. Sacks</name><affiliation wicri:level="1"><nlm:affiliation>Nutrition Department, Harvard T. H. Chan School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02478, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Nutrition Department, Harvard T. H. Chan School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02478</wicri:regionArea><wicri:noRegion>Massachusetts 02478</wicri:noRegion></affiliation></author><author><name sortKey="Tardif, Jean Claude" sort="Tardif, Jean Claude" uniqKey="Tardif J" first="Jean-Claude" last="Tardif">Jean-Claude Tardif</name><affiliation wicri:level="1"><nlm:affiliation>Montreal Heart Institute, Université de Montréal, 5000 Belanger Street, Montréal, Québec H1T 1C8, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Montreal Heart Institute, Université de Montréal, 5000 Belanger Street, Montréal, Québec H1T 1C8</wicri:regionArea><wicri:noRegion>Québec H1T 1C8</wicri:noRegion></affiliation></author><author><name sortKey="Hegele, Robert A" sort="Hegele, Robert A" uniqKey="Hegele R" first="Robert A" last="Hegele">Robert A. Hegele</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine and Robarts Research Institute, Western University, 4288A-1151 Richmond Street North, London, Ontario N6A 5B7, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medicine and Robarts Research Institute, Western University, 4288A-1151 Richmond Street North, London, Ontario N6A 5B7</wicri:regionArea><wicri:noRegion>Ontario N6A 5B7</wicri:noRegion></affiliation></author></analytic><series><title level="j">Nature reviews. Cardiology</title><idno type="eISSN">1759-5010</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Plasma levels of HDL cholesterol (HDL-C) predict the risk of cardiovascular disease at the epidemiological level, but a direct causal role for HDL in cardiovascular disease remains controversial. Studies in animal models and humans with rare monogenic disorders link only particular HDL-associated mechanisms with causality, including those mechanisms related to particle functionality rather than cholesterol content. Mendelian randomization studies indicate that most genetic variants that affect a range of pathways that increase plasma HDL-C levels are not usually associated with reduced risk of cardiovascular disease, with some exceptions, such as cholesteryl ester transfer protein variants. Furthermore, only a fraction of HDL-C variation has been explained by known loci from genome-wide association studies (GWAS), suggesting the existence of additional pathways and targets. Systems genetics can enhance our understanding of the spectrum of HDL pathways, particularly those pathways that involve new and non-obvious GWAS loci. Bioinformatic approaches can also define new molecular interactions inferred from both large-scale genotypic data and RNA sequencing data to reveal biologically meaningful gene modules and networks governing HDL metabolism with direct relevance to disease end points. Targeting these newly recognized causal networks might inform the development of novel therapeutic strategies to reduce the risk of cardiovascular disease.</div></front></TEI><affiliations><list><country><li>Australie</li><li>Canada</li><li>France</li><li>Suisse</li><li>États-Unis</li></country><region><li>District de Columbia</li><li>Île-de-France</li></region><settlement><li>Paris</li></settlement></list><tree><country name="États-Unis"><noRegion><name sortKey="Rosenson, Robert S" sort="Rosenson, Robert S" uniqKey="Rosenson R" first="Robert S" last="Rosenson">Robert S. Rosenson</name></noRegion><name sortKey="Bjorkegren, Johan L M" sort="Bjorkegren, Johan L M" uniqKey="Bjorkegren J" first="Johan L M" last="Björkegren">Johan L M. Björkegren</name><name sortKey="Brewer, H Bryan" sort="Brewer, H Bryan" uniqKey="Brewer H" first="H Bryan" last="Brewer">H Bryan Brewer</name><name sortKey="Kim, Daniel Seung" sort="Kim, Daniel Seung" uniqKey="Kim D" first="Daniel Seung" last="Kim">Daniel Seung Kim</name><name sortKey="Sacks, Frank M" sort="Sacks, Frank M" uniqKey="Sacks F" first="Frank M" last="Sacks">Frank M. Sacks</name></country><country name="Australie"><noRegion><name sortKey="Barter, Philip J" sort="Barter, Philip J" uniqKey="Barter P" first="Philip J" last="Barter">Philip J. 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Hegele</name><name sortKey="Tardif, Jean Claude" sort="Tardif, Jean Claude" uniqKey="Tardif J" first="Jean-Claude" last="Tardif">Jean-Claude Tardif</name></country><country name="Suisse"><noRegion><name sortKey="Niesor, Eric" sort="Niesor, Eric" uniqKey="Niesor E" first="Eric" last="Niesor">Eric Niesor</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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