Singh, Srijan, Frydrysiak-Brzozowska, Adrianna, Michie, Colin ORCID: 0009-0003-6642-3057, Ayad, Aimen E Ben, Khasanova, Saida S and Bordon, Jeremias (2024) A Primer on Epigenetic Changes: The More We Know, the More We Find in Fetuses and Infants. Newborn, 3 (3). pp. 219-232. ISSN 2769-514X
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Official URL: https://doi.org/10.5005/jp-journals-11002-0104
Abstract
Epigenetics is the study of heritable traits that happen without changes to the DNA sequence. The Greek prefix epi- implies features that modify the traditional genetic mechanisms of inheritance. Increasing information underscores the importance of epigenetic changes during the fetal period and infancy. The most frequently seen epigenetic changes are mediated via DNA methylation, changes in gene expression due to non-coding RNAs, and post-translational modifications of histone proteins. DNA methylation can be confirmed using methods such as bisulfite treatment, enzyme sensitivity assays, and antibody specificity-based techniques. Histone modifications are typically detected through antibody recognition. Chromatin immunoprecipitation (ChIP) is an antibody-based technology to selectively enrich specific DNA-binding proteins along with their DNA
targets. Since epigenetic alterations are often reversible, modifying epigenetic marks contributing to disease development may provide an approach to designing new therapies. Gene hypermethylation and histone hypoacetylation are attractive targets for the treatment of epigenetic diseases because these epigenetic alterations are reversible. The first 1000 days of life, from conception through infancy, comprise the most-likely timeperiod for environmental exposures and nutrition to exert beneficial/potentially harmful epigenetic effects. During this period, a typical metabolic reprogramming induced by extrinsic factors such as allergens, viruses, pollutants, diet, or microbiome might drive cellular metabolic dysfunctions and defective immune responses in allergic diseases. Epigenetics also plays a role in the developmental origins of adult metabolic diseases.
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