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首页> 外文期刊>Cell metabolism >Hypothalamic mTORC1 signaling controls sympathetic nerve activity and arterial pressure and mediates leptin effects
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Hypothalamic mTORC1 signaling controls sympathetic nerve activity and arterial pressure and mediates leptin effects

机译：下丘脑mTORC1信号控制交感神经活动和动脉压并介导瘦素作用

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The fundamental importance of the hypothalamus in the regulation of autonomic and cardiovascular functions is well established. However, the molecular processes involved are not well understood. Here, we show that the mammalian (or mechanistic) target of rapamycin (mTOR) signaling in the hypothalamus is tied to the activity of the sympathetic nervous system and to cardiovascular function. Modulation of mTOR complex 1 (mTORC1) signaling caused dramatic changes in sympathetic traffic, blood flow, and arterial pressure. Our data also demonstrate the importance of hypothalamic mTORC1 signaling in transducing the sympathetic and cardiovascular actions of leptin. Moreover, we show that the PI3K pathway links the leptin receptor to mTORC1 signaling and that changes in its activity impact sympathetic traffic and arterial pressure. These findings establish mTORC1 activity in the hypothalamus as a key determinant of sympathetic and cardiovascular regulation and suggest that dysregulated hypothalamic mTORC1 activity may influence the development of cardiovascular diseases.
机译：下丘脑在调节自主神经功能和心血管功能方面的根本重要性已得到公认。然而，所涉及的分子过程尚未被很好地理解。在这里，我们表明，下丘脑中雷帕霉素（mTOR）信号的哺乳动物（或机制）靶标与交感神经系统的活动和心血管功能相关。 mTOR复合物1（mTORC1）信号的调节引起交感神经通畅，血流量和动脉压的急剧变化。我们的数据还证明了下丘脑mTORC1信号转导瘦素的交感和心血管作用的重要性。此外，我们表明PI3K途径将瘦素受体链接到mTORC1信号传导，其活动的变化影响交感神经交通和动脉压。这些发现将下丘脑中的mTORC1活性确定为交感和心血管调节的关键决定因素，并表明下丘脑mTORC1活性失调可能影响心血管疾病的发展。

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