Advance in the mechanisms underlying prenatal stress-induced depressive-like behavior in offspring

Kaixuan Xu , Dongli Song , Hui Li , Yushan Lu , Zhongliang Zhu
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引用次数: 0

Abstract

Prenatal stress (PS) represents a critical environmental factor that causes developmental disruptions in offspring, characterized by multisystemic vulnerabilities across neuropsychiatric, cardiovascular, metabolic, and immunological domains. Through intricate embryonic reprogramming mechanisms, PS alters brain developmental trajectories and physiological regulatory networks, resulting in increased long-term risks for neurodevelopmental disorders, particularly depressive-like behavior. PS causes dysregulation in multiple physiological processes, including hypothalamic-pituitary-adrenal (HPA) axis activation, epigenetic modifications, neurotransmitter systems, brain-derived neurotrophic factor (BDNF), gut microbiota, and neuroimmune responses. Additionally, genetic factors, sex specificity, and critical developmental windows further complicate the PS-mediated onset of depressive-like behavior. Here, we review clinical and animal studies and analyze how the multiple mechanisms form complex regulatory networks during intrauterine development, leading to long-lasting psychopathological effects in offspring.
产前应激诱导的后代抑郁样行为机制研究进展
产前应激(PS)是导致后代发育中断的关键环境因素,其特征是神经精神、心血管、代谢和免疫领域的多系统脆弱性。通过复杂的胚胎重编程机制,PS改变了大脑发育轨迹和生理调节网络,导致神经发育障碍,特别是抑郁样行为的长期风险增加。PS导致多种生理过程失调,包括下丘脑-垂体-肾上腺(HPA)轴激活、表观遗传修饰、神经递质系统、脑源性神经营养因子(BDNF)、肠道微生物群和神经免疫反应。此外,遗传因素、性别特异性和关键发育窗口进一步使ps介导的抑郁样行为发病复杂化。在此,我们回顾了临床和动物研究,并分析了多种机制如何在宫内发育过程中形成复杂的调节网络,从而对后代产生长期的精神病理影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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