Germ Cell Drivers: Transmission of Preconception Stress Across Generations.
Germ Cell Drivers: Transmission of Preconception Stress Across Generations.
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生殖细胞驱动因素：跨代的孕前压力传递。
DOI：
10.3389/fnhum.2021.642762
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发表时间：
2021
影响因子：
2.9
通讯作者：
Epperson CN
中科院分区：
文献类型：
--
作者：
Duffy KA;Bale TL;Epperson CN
暴露在压力下可以加速成熟和加速繁殖。虽然具有潜在的适应性，但代价是更高的发病率和死亡率。在人类中，压力的代际效应已经得到证实，但确切的机制尚不清楚。引人注目的是，即使父母在怀孕前就有压力，成年后，他们的后代也会表现出更差的心理和身体健康。主要来自临床前模型的新证据表明，表观遗传编程可能编码生殖细胞孕前应激暴露，潜在地影响后代的表型。在这篇叙述性综述中，我们评估了这种机制在动物和人类中男性和女性的证据强度。最有力的证据来自对雄性小鼠的研究，在这些研究中，父亲的孕前应激与后代的许多表型变化有关，并且涉及到应激引起的精子中小非编码RNA含量的变化。最近对男性的两项研究提供了证据，证明精子中的一些小的非编码rna对过去和现在的压力有反应，包括在老鼠身上发现的一些相同的rna。尽管初步证据表明，小鼠的研究结果可能适用于男性，但接下来的步骤将是(1)考虑应激类型、严重程度、持续时间和发育时间是否影响生殖细胞表观遗传标记，(2)确定生殖细胞表观遗传标记是否与应激暴露父母后代的疾病风险有关，以及(3)克服方法上的挑战，以便将这项研究扩展到女性。
Exposure to stress can accelerate maturation and hasten reproduction. Although potentially adaptive, the trade-off is higher risk for morbidity and mortality. In humans, the intergenerational effects of stress have been demonstrated, but the precise mechanisms are unknown. Strikingly, even if parental stress occurs prior to conception, as adults, their offspring show worse mental and physical health. Emerging evidence primarily from preclinical models suggests that epigenetic programming may encode preconception stress exposures in germ cells, potentially impacting the phenotype of the offspring. In this narrative review, we evaluate the strength of the evidence for this mechanism across animals and humans in both males and females. The strongest evidence comes from studies of male mice, in which paternal preconception stress is associated with a host of phenotypic changes in the offspring and stress-induced changes in the small non-coding RNA content in sperm have been implicated. Two recent studies in men provide evidence that some small non-coding RNAs in sperm are responsive to past and current stress, including some of the same ones identified in mice. Although preliminary evidence suggests that findings from mice may map onto men, the next steps will be (1) considering whether stress type, severity, duration, and developmental timing affect germ cell epigenetic markers, (2) determining whether germ cell epigenetic markers contribute to disease risk in the offspring of stress-exposed parents, and (3) overcoming methodological challenges in order to extend this research to females.
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