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DNA methylation: a potential mediator between air pollution and metabolic syndrome

Given the global increase in air pollution and its crucial role in human health, as well as the steep rise in prevalence of metabolic syndrome (MetS), a better understanding of the underlying mechanisms by which environmental pollution may influence MetS is imperative. Exposure to air pollution is k...

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Autores principales: Poursafa, Parinaz, Kamali, Zoha, Fraszczyk, Eliza, Boezen, H. Marike, Vaez, Ahmad, Snieder, Harold
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9245491/
https://www.ncbi.nlm.nih.gov/pubmed/35773726
http://dx.doi.org/10.1186/s13148-022-01301-y
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author Poursafa, Parinaz
Kamali, Zoha
Fraszczyk, Eliza
Boezen, H. Marike
Vaez, Ahmad
Snieder, Harold
author_facet Poursafa, Parinaz
Kamali, Zoha
Fraszczyk, Eliza
Boezen, H. Marike
Vaez, Ahmad
Snieder, Harold
author_sort Poursafa, Parinaz
collection PubMed
description Given the global increase in air pollution and its crucial role in human health, as well as the steep rise in prevalence of metabolic syndrome (MetS), a better understanding of the underlying mechanisms by which environmental pollution may influence MetS is imperative. Exposure to air pollution is known to impact DNA methylation, which in turn may affect human health. This paper comprehensively reviews the evidence for the hypothesis that the effect of air pollution on the MetS is mediated by DNA methylation in blood. First, we present a summary of the impact of air pollution on metabolic dysregulation, including the components of MetS, i.e., disorders in blood glucose, lipid profile, blood pressure, and obesity. Then, we provide evidence on the relation between air pollution and endothelial dysfunction as one possible mechanism underlying the relation between air pollution and MetS. Subsequently, we review the evidence that air pollution (PM, ozone, NO(2) and PAHs) influences DNA methylation. Finally, we summarize association studies between DNA methylation and MetS. Integration of current evidence supports our hypothesis that methylation may partly mediate the effect of air pollution on MetS. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13148-022-01301-y.
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spelling pubmed-92454912022-07-01 DNA methylation: a potential mediator between air pollution and metabolic syndrome Poursafa, Parinaz Kamali, Zoha Fraszczyk, Eliza Boezen, H. Marike Vaez, Ahmad Snieder, Harold Clin Epigenetics Review Given the global increase in air pollution and its crucial role in human health, as well as the steep rise in prevalence of metabolic syndrome (MetS), a better understanding of the underlying mechanisms by which environmental pollution may influence MetS is imperative. Exposure to air pollution is known to impact DNA methylation, which in turn may affect human health. This paper comprehensively reviews the evidence for the hypothesis that the effect of air pollution on the MetS is mediated by DNA methylation in blood. First, we present a summary of the impact of air pollution on metabolic dysregulation, including the components of MetS, i.e., disorders in blood glucose, lipid profile, blood pressure, and obesity. Then, we provide evidence on the relation between air pollution and endothelial dysfunction as one possible mechanism underlying the relation between air pollution and MetS. Subsequently, we review the evidence that air pollution (PM, ozone, NO(2) and PAHs) influences DNA methylation. Finally, we summarize association studies between DNA methylation and MetS. Integration of current evidence supports our hypothesis that methylation may partly mediate the effect of air pollution on MetS. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13148-022-01301-y. BioMed Central 2022-06-30 /pmc/articles/PMC9245491/ /pubmed/35773726 http://dx.doi.org/10.1186/s13148-022-01301-y Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Poursafa, Parinaz
Kamali, Zoha
Fraszczyk, Eliza
Boezen, H. Marike
Vaez, Ahmad
Snieder, Harold
DNA methylation: a potential mediator between air pollution and metabolic syndrome
title DNA methylation: a potential mediator between air pollution and metabolic syndrome
title_full DNA methylation: a potential mediator between air pollution and metabolic syndrome
title_fullStr DNA methylation: a potential mediator between air pollution and metabolic syndrome
title_full_unstemmed DNA methylation: a potential mediator between air pollution and metabolic syndrome
title_short DNA methylation: a potential mediator between air pollution and metabolic syndrome
title_sort dna methylation: a potential mediator between air pollution and metabolic syndrome
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9245491/
https://www.ncbi.nlm.nih.gov/pubmed/35773726
http://dx.doi.org/10.1186/s13148-022-01301-y
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