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Genetic Programming of Hypertension

The heritability of hypertension (HTN) is widely recognized and as a result, extensive studies ranging from genetic linkage analyses to genome-wide association studies are actively ongoing to elucidate the etiology of both monogenic and polygenic forms of HTN. Due to the complex nature of essential...

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Autores principales: Ahn, Sun-Young, Gupta, Charu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5786744/
https://www.ncbi.nlm.nih.gov/pubmed/29404309
http://dx.doi.org/10.3389/fped.2017.00285
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author Ahn, Sun-Young
Gupta, Charu
author_facet Ahn, Sun-Young
Gupta, Charu
author_sort Ahn, Sun-Young
collection PubMed
description The heritability of hypertension (HTN) is widely recognized and as a result, extensive studies ranging from genetic linkage analyses to genome-wide association studies are actively ongoing to elucidate the etiology of both monogenic and polygenic forms of HTN. Due to the complex nature of essential HTN, however, single genes affecting blood pressure (BP) variability remain difficult to isolate and identify and have rendered the development of single-gene targeted therapies challenging. The roles of other causative factors in modulating BP, such as gene–environment interactions and epigenetic factors, are increasingly being brought to the forefront. In this review, we discuss the various monogenic HTN syndromes and corresponding pathophysiologic mechanisms, the different methodologies employed in genetic studies of essential HTN, the mechanisms for epigenetic modulation of essential HTN, pharmacogenomics and HTN, and finally, recent advances in genetic studies of essential HTN in the pediatric population.
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spelling pubmed-57867442018-02-05 Genetic Programming of Hypertension Ahn, Sun-Young Gupta, Charu Front Pediatr Pediatrics The heritability of hypertension (HTN) is widely recognized and as a result, extensive studies ranging from genetic linkage analyses to genome-wide association studies are actively ongoing to elucidate the etiology of both monogenic and polygenic forms of HTN. Due to the complex nature of essential HTN, however, single genes affecting blood pressure (BP) variability remain difficult to isolate and identify and have rendered the development of single-gene targeted therapies challenging. The roles of other causative factors in modulating BP, such as gene–environment interactions and epigenetic factors, are increasingly being brought to the forefront. In this review, we discuss the various monogenic HTN syndromes and corresponding pathophysiologic mechanisms, the different methodologies employed in genetic studies of essential HTN, the mechanisms for epigenetic modulation of essential HTN, pharmacogenomics and HTN, and finally, recent advances in genetic studies of essential HTN in the pediatric population. Frontiers Media S.A. 2018-01-22 /pmc/articles/PMC5786744/ /pubmed/29404309 http://dx.doi.org/10.3389/fped.2017.00285 Text en Copyright © 2018 Ahn and Gupta. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pediatrics
Ahn, Sun-Young
Gupta, Charu
Genetic Programming of Hypertension
title Genetic Programming of Hypertension
title_full Genetic Programming of Hypertension
title_fullStr Genetic Programming of Hypertension
title_full_unstemmed Genetic Programming of Hypertension
title_short Genetic Programming of Hypertension
title_sort genetic programming of hypertension
topic Pediatrics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5786744/
https://www.ncbi.nlm.nih.gov/pubmed/29404309
http://dx.doi.org/10.3389/fped.2017.00285
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