期刊
ALCOHOL-CLINICAL AND EXPERIMENTAL RESEARCH
卷 47, 期 1, 页码 18-35出版社
WILEY
DOI: 10.1111/acer.14972
关键词
epigenetic; fetal alcohol; stress axis
Using publicly available gene expression datasets, we conducted a systematic review with meta-analytic elements to determine the role of epigenetic mechanisms in prenatal alcohol exposure-induced dysfunctions in the hypothalamic-pituitary-adrenal (HPA) axis in offspring. Our network analysis identified key pathways associated with alcohol-mediated epigenetic alterations and provided insights into the developmental effects of alcohol on the HPA axis.
We conducted a systematic review with meta-analytic elements using publicly available Gene Expression Omnibus (GEO) datasets to determine the role of epigenetic mechanisms in prenatal alcohol exposure (PAE)-induced hypothalamic-pituitary-adrenal (HPA) axis dysfunctions in offspring. Several studies have demonstrated that PAE has long-term consequences on HPA axis functions in offspring. Some studies determined that alcohol-induced epigenetic alterations during fetal development persist in adulthood. However, additional research is needed to understand the major epigenetic events leading to alcohol-induced teratogenesis of the HPA axis. Our network analysis of GEO datasets identified key pathways relevant to alcohol-mediated histone modifications, DNA methylation, and miRNA involvement associated with PAE-induced alterations of the HPA axis. Our analysis indicated that PAE perturbated the epigenetic machinery to activate corticotrophin-releasing hormone, while it suppressed opioid, glucocorticoid receptor, and circadian clock genes. These results help to further our understanding of the epigenetic basis of alcohol's effects on HPA axis development.
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