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首页> 外文期刊>Frontiers in neuroendocrinology >Disruption of fetal hormonal programming (prenatal stress) implicates shared risk for sex differences in depression and cardiovascular disease
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Disruption of fetal hormonal programming (prenatal stress) implicates shared risk for sex differences in depression and cardiovascular disease

机译：胎儿激素编程的中断（产前压力）意味着抑郁症和心血管疾病的性别差异有共同的风险

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Comorbidity of major depressive disorder (MDD) and cardiovascular disease (CVD) represents the fourth leading cause of morbidity and mortality worldwide, and women have a two times greater risk than men. Thus understanding the pathophysiology has widespread implications for attenuation and prevention of disease burden. We suggest that sex-dependent MDD-CVD comorbidity may result from alterations in fetal programming consequent to the prenatal maternal environments that produce excess glucocorticoids, which then drive sex-dependent developmental alterations of the fetal hypothalamic-pituitary-adrenal (HPA) axis circuitry impacting mood, stress regulation, autonomic nervous system (ANS), and the vasculature in adulthood. Evidence is consistent with the hypothesis that disruptions of pathways associated with gamma aminobutyric acid (GABA) in neuronal and vascular development and growth factors have critical roles in key developmental periods and adult responses to injury in heart and brain. Understanding the potential fetal origins of these sex differences will contribute to development of novel sex-dependent therapeutics.
机译：重度抑郁症（MDD）和心血管疾病（CVD）的合并症是全世界发病率和死亡率的第四大主要原因，女性的危险性是男性的两倍。因此，了解病理生理学对减轻和预防疾病负担具有广泛的意义。我们建议性别相关的MDD-CVD合并症可能是由胎儿程序改变引起的，其原因是产前产妇环境产生了过多的糖皮质激素，继而驱动胎儿下丘脑-垂体-肾上腺（HPA）轴电路的性别依赖性发育改变情绪，压力调节，自主神经系统（ANS）和成年后的脉管系统。证据与以下假设相符：在神经发育和血管生长发育因子中，与γ-氨基丁酸（GABA）相关的通路的破坏在关键的发育时期以及成人对心脏和脑部损伤的反应中起着至关重要的作用。了解这些性别差异的潜在胎儿起源将有助于新型性别依赖疗法的发展。

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