Nrf2 contributes to the weight gain of mice during space travel
Nrf2 contributes to the weight gain of mice during space travel
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DOI：
10.1038/s42003-020-01227-2
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发表时间：
2020-09-08
影响因子：
5.9
通讯作者：
Yamamoto, Masayuki
中科院分区：
文献类型：
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作者：
Suzuki, Takafumi;Uruno, Akira;Yamamoto, Masayuki
太空飞行会产生一个具有独特压力源的极端环境，但我们对我们的身体如何应对这些压力知之甚少。虽然飞行中的太空研究存在许多棘手的限制，但有些可以通过利用基因敲除疾病模型小鼠来克服。在这里，我们报告了 Nrf2（压力防御途径的主要调节因子）的缺失如何影响被运送到国际空间站 (ISS) 的小鼠的健康。在国际空间站停留 31 天后，所有飞行小鼠均安全返回地球。转录组和代谢组分析表明，太空旅行的压力会引起血浆代谢物的类衰老变化，并激活 Nrf2 信号通路。特别是，Nrf2被发现对于维持白色脂肪组织的稳态很重要。这项研究为利用小鼠基因敲除疾病模型进行未来太空研究开辟了途径，并为减轻限制人类进一步探索太空的太空引起的压力提供了见解。 Suzuki、Uruno、Yumoto 等人使用 Nrf2 敲除小鼠。研究表明，太空旅行激活了 Nrf2 信号传导，该信号通过调节白色脂肪组织的脂肪代谢来促进小鼠体重增加。这项研究提供了对减轻太空旅行压力的潜在干预措施的见解。
Space flight produces an extreme environment with unique stressors, but little is known about how our body responds to these stresses. While there are many intractable limitations for in-flight space research, some can be overcome by utilizing gene knockout-disease model mice. Here, we report how deletion of Nrf2, a master regulator of stress defense pathways, affects the health of mice transported for a stay in the International Space Station (ISS). After 31 days in the ISS, all flight mice returned safely to Earth. Transcriptome and metabolome analyses revealed that the stresses of space travel evoked ageing-like changes of plasma metabolites and activated the Nrf2 signaling pathway. Especially, Nrf2 was found to be important for maintaining homeostasis of white adipose tissues. This study opens approaches for future space research utilizing murine gene knockout-disease models, and provides insights into mitigating space-induced stresses that limit the further exploration of space by humans. Using Nrf2 knockout mice, Suzuki, Uruno, Yumoto et al. show that space travel activates Nrf2 signaling, which contributes to the weight gain of mice by regulating fat metabolism of white adipose tissues. This study provides insights into potential interventions to mitigate stresses that accompany space travels.