Epigenome-wide association studies of allergic disease and the environment

Fadadu, Raj P.; Koppelman, Gerard H.

doi:10.1016/j.jaci.2023.05.020

Cited by 13 publications

(2 citation statements)

References 80 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A very good example is the dramatic increase in the prevalence of these diseases that occurred in the second half of the past century. This rapid increase indicates that the changes cannot have a purely genetic origin and that the interaction between the modifying environment and the individual genome, which may make some people more prone to disease, should be considered ( 6 , 7 ). This consideration is mainly related to the more frequent atopic diseases and may not be so applicable to others, the origins of which might be different.…”

Section: Epidemiologymentioning

confidence: 99%

Grand challenges in genetics and epidemiology of allergic diseases: from genome to exposome and back

Garcia-Marcos

2024

Front. Allergy

View full text Add to dashboard Cite

Section: Epidemiologymentioning

confidence: 99%

Grand challenges in genetics and epidemiology of allergic diseases: from genome to exposome and back

Garcia-Marcos

2024

Front. Allergy

View full text Add to dashboard Cite

“…Epigenetic modifications have been extensively associated with asthma and allergic diseases. These associations have been previously reviewed [ 40 , 41 ] and are not the focus of this paper. It is important to consider that associations between exposures, epigenetic modifications, and disease phenotypes do not equate with demonstrating causality or pathogenesis, as these epigenetic modifications may be secondary to the development of the phenotype ( Figure 1 ).…”

Section: Introductionmentioning

confidence: 99%

A Review of the Epigenetic Clock: Emerging Biomarkers for Asthma and Allergic Disease

Vasileva,

Greenwood,

Daley

2023

Genes

View full text Add to dashboard Cite

DNA methylation (DNAm) is a dynamic, age-dependent epigenetic modification that can be used to study interactions between genetic and environmental factors. Environmental exposures during critical periods of growth and development may alter DNAm patterns, leading to increased susceptibility to diseases such as asthma and allergies. One method to study the role of DNAm is the epigenetic clock—an algorithm that uses DNAm levels at select age-informative Cytosine-phosphate-Guanine (CpG) dinucleotides to predict epigenetic age (EA). The difference between EA and calendar age (CA) is termed epigenetic age acceleration (EAA) and reveals information about the biological capacity of an individual. Associations between EAA and disease susceptibility have been demonstrated for a variety of age-related conditions and, more recently, phenotypes such as asthma and allergic diseases, which often begin in childhood and progress throughout the lifespan. In this review, we explore different epigenetic clocks and how they have been applied, particularly as related to childhood asthma. We delve into how in utero and early life exposures (e.g., smoking, air pollution, maternal BMI) result in methylation changes. Furthermore, we explore the potential for EAA to be used as a biomarker for asthma and allergic diseases and identify areas for further study.

show abstract

The Association Study of Targeted DNA Methylation and Thrombophilia

Kui,

Feng,

Leng

et al. 2024

Indian J Hematol Blood Transfus

View full text Add to dashboard Cite

Objective The aim of this study is to investigate the relationship of leukocytes DNA methylation in targeted sites and thrombophilia. Methods Eight thrombophilia patients and their kin-related individuals as the healthy control. Targeted DNA methylation from peripheral leukocytes were examined with MassArray. Multivariate correlation analysis was used to estimate targeted gene methylation as an independent risk factor of thrombophilia. Receiver operating characteristic curve analysis was used to calculate the accuracy of biomarkers in the prediction of thrombophilia. Results The age of thrombophilia group was higher than control group (P < 0.001). F5.24.CpG.10 and Protein S.44.CpG.29–33 methylation were significantly associated with thrombophilia negatively and positively (r = -0.7289, P < 0.01 and r = 0.5667, P < 0.05). F5.24.CpG.10 methylation was higher in control group (P < 0.01), but Protein S.44.CpG.29–33 methylation increased in thrombophilia group (P < 0.05). The areas under curve of ROC were 0.9297 and 0.8437, respectively. Conclusion Target DNA methylation in Protein S.44.CpG.29–33 island is associated with an elevated risk of thrombophilia.

show abstract

Epigenome-wide association studies of allergic disease and the environment

Cited by 13 publications

References 80 publications

Grand challenges in genetics and epidemiology of allergic diseases: from genome to exposome and back

Grand challenges in genetics and epidemiology of allergic diseases: from genome to exposome and back

A Review of the Epigenetic Clock: Emerging Biomarkers for Asthma and Allergic Disease

The Association Study of Targeted DNA Methylation and Thrombophilia

Contact Info

Product

Resources

About