Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape.
Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape.
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DOI：
10.3390/nu13113857
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发表时间：
2021-10-28
期刊：
影响因子：
5.9
通讯作者：
Tran PV
中科院分区：
文献类型：
--
作者：
Barks AK;Liu SX;Georgieff MK;Hallstrom TC;Tran PV
缺铁性贫血（ID）是世界上最重要的微量营养素缺乏症，影响约40%的孕妇和幼儿。产前和产后早期的ID对神经发育有明显的影响，导致长期影响，如认知障碍和神经精神疾病的风险增加。ID的治疗一直很复杂，因为它并不总是解决长期的神经发育缺陷。在动物模型中，发育性ID导致与神经传递和突触可塑性相关的基因失调相关的海马结构和功能异常。这些基因的失调是一个可能的近因终身赤字，以下发展ID。然而，铁和基因失调之间的直接功能联系尚未得到阐明。铁依赖性表观遗传修饰是ID在整个生命周期中改变基因表达的一种机制。JARID蛋白和泰特蛋白是铁依赖性表观遗传修饰剂的两个家族，它们通过在脑发育的关键时期建立适当的基因调控，在神经发育过程中发挥关键作用。因此，JARID和TTRID可以促进铁介导的表观遗传机制，通过该机制，早期ID直接导致整个生命周期中基因调控的稳定变化。
Iron deficiency (ID) anemia is the foremost micronutrient deficiency worldwide, affecting around 40% of pregnant women and young children. ID during the prenatal and early postnatal periods has a pronounced effect on neurodevelopment, resulting in long-term effects such as cognitive impairment and increased risk for neuropsychiatric disorders. Treatment of ID has been complicated as it does not always resolve the long-lasting neurodevelopmental deficits. In animal models, developmental ID results in abnormal hippocampal structure and function associated with dysregulation of genes involved in neurotransmission and synaptic plasticity. Dysregulation of these genes is a likely proximate cause of the life-long deficits that follow developmental ID. However, a direct functional link between iron and gene dysregulation has yet to be elucidated. Iron-dependent epigenetic modifications are one mechanism by which ID could alter gene expression across the lifespan. The jumonji and AT-rich interaction domain-containing (JARID) protein and the Ten-Eleven Translocation (TET) proteins are two families of iron-dependent epigenetic modifiers that play critical roles during neural development by establishing proper gene regulation during critical periods of brain development. Therefore, JARIDs and TETs can contribute to the iron-mediated epigenetic mechanisms by which early-life ID directly causes stable changes in gene regulation across the life span.
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影响因子：
64.5
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