表观遗传学
胎儿
医学
DNA甲基化
胎盘
疾病
宫内生长受限
怀孕
内分泌学
内科学
生理学
生物信息学
基因表达
生物
基因
遗传学
作者
Carlos Briceño‐Pérez,Liliana Briceño‐Sanabria,Carlos Briceño‐Sanabria,Eduardo Reyna‐Villasmil
摘要
Abstract The relationship between events occurring during intrauterine development and later‐life predisposition to long‐term disease, has been described. The fetus responds to excess intrauterine exposure to high levels of corticosteroids, modifying their physiological development and stopping their growth. Fetal exposure to elevated levels of either endogenous (alterations in fetal hypothalamic‐pituitary‐adrenal axis) or synthetic corticosteroids, is one model of early‐life adversity; to developing adult disease. At the molecular level, there are transcriptional changes in metabolic and growth pathways. Epigenetic mechanisms participate in transgenerational inheritance, not genomic. Exposures that change 11β‐hydroxysteroid dehydrogenase type 2 enzyme methylation status in the placenta can result in transcriptional repression of the gene, causing the fetus to be exposed to higher levels of cortisol. More precise diagnosis and management of antenatal corticosteroids for preterm birth, would potentially decrease the risk of long‐term adverse outcomes. More studies are needed to understand the potential roles of factors to alter fetal corticosteroid exposure. Long‐term infant follow‐up is required to determine whether methylation changes in placenta may represent useful biomarkers of later disease risk. This review, summarize recent advances in the programming of fetal effects of corticosteroid exposure, the role of corticosteroids in epigenetic gene regulation of placental 11β‐hydroxysteroid dehydrogenase type 2 enzyme expression and transgenerational effects.
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