Developmental origins of cardiovascular disease: Impact of early life stress in humans and rodents.
Developmental origins of cardiovascular disease: Impact of early life stress in humans and rodents.
复制标题
心血管疾病的发育起源：早期生活压力对人类和啮齿动物的影响。
DOI：
10.1016/j.neubiorev.2016.07.018
复制
发表时间：
2017-03
影响因子：
8.2
通讯作者：
Loria AS
中科院分区：
文献类型：
--
作者：
Murphy MO;Cohn DM;Loria AS
健康与疾病的发展起源（DOHaD）假设童年时期的环境侮辱会使个体在成年后患上慢性疾病。新出现的流行病学数据有力地支持，暴露于不良童年经历的早期生活压力（ELS）被视为能够预测未来心血管疾病风险的独立风险因素。利用产后生活中的慢性行为应激，特别是母亲分离（MatSep）的实验动物模型，为阐明ELS增加包括高血压在内的心血管疾病风险的分子机制提供了合适的工具。本综述的目的是强调当前流行病学研究将ELS与心血管疾病的发展联系起来，并讨论从动物研究中确定的潜在分子机制。总之，这篇综述揭示了未来的研究需要进一步阐明ELS的分子机制，以便开发更个性化的治疗方法来减轻成年期慢性行为应激（包括心血管和心脏疾病）的长期后果。
The Developmental Origins of Health and Disease (DOHaD) hypothesizes that environmental insults during childhood programs the individual to develop chronic disease in adulthood. Emerging epidemiological data strongly supports that early life stress (ELS) given by the exposure to adverse childhood experiences is regarded as an independent risk factor capable of predicting future risk of cardiovascular disease. Experimental animal models utilizing chronic behavioral stress during postnatal life, specifically maternal separation (MatSep) provides a suitable tool to elucidate molecular mechanisms by which ELS increases the risk to develop cardiovascular disease, including hypertension. The purpose of this review is to highlight current epidemiological studies linking ELS to the development of cardiovascular disease and to discuss the potential molecular mechanisms identified from animal studies. Overall, this review reveals the need for future investigations to further clarify the molecular mechanisms of ELS in order to develop more personalized therapeutics to mitigate the long-term consequences of chronic behavioral stress including cardiovascular and heart disease in adulthood.