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Genome-Wide Association Studies in Atherosclerosis

Cardiovascular disease remains the major cause of worldwide morbidity and mortality. Its pathophysiology is complex and multifactorial. Because the phenotype of cardiovascular disease often shows a marked heritable pattern, it is likely that genetic factors play an important role. In recent years, l...

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Autores principales: Sivapalaratnam, S., Motazacker, M. M., Maiwald, S., Hovingh, G. K., Kastelein, J. J. P., Levi, M., Trip, M. D., Dallinga-Thie, G. M.
Formato: Texto
Lenguaje:English
Publicado: Current Science Inc. 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085784/
https://www.ncbi.nlm.nih.gov/pubmed/21369780
http://dx.doi.org/10.1007/s11883-011-0173-4
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author Sivapalaratnam, S.
Motazacker, M. M.
Maiwald, S.
Hovingh, G. K.
Kastelein, J. J. P.
Levi, M.
Trip, M. D.
Dallinga-Thie, G. M.
author_facet Sivapalaratnam, S.
Motazacker, M. M.
Maiwald, S.
Hovingh, G. K.
Kastelein, J. J. P.
Levi, M.
Trip, M. D.
Dallinga-Thie, G. M.
author_sort Sivapalaratnam, S.
collection PubMed
description Cardiovascular disease remains the major cause of worldwide morbidity and mortality. Its pathophysiology is complex and multifactorial. Because the phenotype of cardiovascular disease often shows a marked heritable pattern, it is likely that genetic factors play an important role. In recent years, large genome-wide association studies have been conducted to decipher the molecular mechanisms underlying this heritable and prevalent phenotype. The emphasis of this review is on the recently identified 17 susceptibility loci for coronary artery disease. Implications of their discovery for biology and clinical medicine are discussed. A description of the landscape of human genetics in the near future in the context of next-generation sequence technologies is provided at the conclusion of this review.
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spelling pubmed-30857842011-06-06 Genome-Wide Association Studies in Atherosclerosis Sivapalaratnam, S. Motazacker, M. M. Maiwald, S. Hovingh, G. K. Kastelein, J. J. P. Levi, M. Trip, M. D. Dallinga-Thie, G. M. Curr Atheroscler Rep Article Cardiovascular disease remains the major cause of worldwide morbidity and mortality. Its pathophysiology is complex and multifactorial. Because the phenotype of cardiovascular disease often shows a marked heritable pattern, it is likely that genetic factors play an important role. In recent years, large genome-wide association studies have been conducted to decipher the molecular mechanisms underlying this heritable and prevalent phenotype. The emphasis of this review is on the recently identified 17 susceptibility loci for coronary artery disease. Implications of their discovery for biology and clinical medicine are discussed. A description of the landscape of human genetics in the near future in the context of next-generation sequence technologies is provided at the conclusion of this review. Current Science Inc. 2011-03-03 2011 /pmc/articles/PMC3085784/ /pubmed/21369780 http://dx.doi.org/10.1007/s11883-011-0173-4 Text en © The Author(s) 2011 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Article
Sivapalaratnam, S.
Motazacker, M. M.
Maiwald, S.
Hovingh, G. K.
Kastelein, J. J. P.
Levi, M.
Trip, M. D.
Dallinga-Thie, G. M.
Genome-Wide Association Studies in Atherosclerosis
title Genome-Wide Association Studies in Atherosclerosis
title_full Genome-Wide Association Studies in Atherosclerosis
title_fullStr Genome-Wide Association Studies in Atherosclerosis
title_full_unstemmed Genome-Wide Association Studies in Atherosclerosis
title_short Genome-Wide Association Studies in Atherosclerosis
title_sort genome-wide association studies in atherosclerosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085784/
https://www.ncbi.nlm.nih.gov/pubmed/21369780
http://dx.doi.org/10.1007/s11883-011-0173-4
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