Loading...
The role of epigenetics in the development of childhood asthma.
Qi, Cancan Xu, Cheng-Jian Koppelman, Gerard H
Qi, Cancan
Xu, Cheng-Jian
Koppelman, Gerard H
Citations
Altmetric:
Advisors
Editors
Other Contributors
Issue Date
2019-11-10
Submitted date
Files
Loading...
Open Access article
Adobe PDF, 1.92 MB
Other Titles
Abstract
Introduction: The development of childhood asthma is caused by a combination of genetic factors and environmental exposures. Epigenetics describes mechanisms of (heritable) regulation of gene expression that occur without changes in DNA sequence. Epigenetics is strongly related to aging, is cell-type specific, and includes DNA methylation, noncoding RNAs, and histone modifications.Areas covered: This review summarizes recent epigenetic studies of childhood asthma in humans, which mostly involve studies of DNA methylation published in the recent five years. Environmental exposures, in particular cigarette smoking, have significant impact on epigenetic changes, but few of these epigenetic signals are also associated with asthma. Several asthma-associated genetic variants relate to DNA methylation. Epigenetic signals can be better understood by studying their correlation with gene expression, which revealed higher presence and activation of blood eosinophils in asthma. Strong associations of nasal methylation signatures and atopic asthma were identified, which were replicable across different populations.Expert commentary: Epigenetic markers have been strongly associated with asthma, and might serve as biomarker of asthma. The causal and longitudinal relationships between epigenetics and disease, and between environmental exposures and epigenetic changes need to be further investigated. Efforts should be made to understand cell-type-specific epigenetic mechanisms in asthma.
Citation
Publisher
Journal
PubMed ID
PubMed Central ID
Additional Links
Embedded video
Type
Other
Language
Description
Review
Series/Report no.
ISSN
1744-8409
EISSN
ISBN
ISMN
Gov't Doc #
Sponsors
License
Attribution-NonCommercial-ShareAlike 4.0 International