Nutrient-sensing mTORC1: Integration of metabolic and autophagic signals.
Nutrient-sensing mTORC1: Integration of metabolic and autophagic signals.
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DOI：
10.1016/j.yjmcc.2016.01.005
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发表时间：
2016-06
影响因子：
5
通讯作者：
Miyamoto S
中科院分区：
文献类型：
--
作者：
Tan VP;Miyamoto S
成年心肌细胞的再生能力是有限的，细胞死亡造成的不可逆转的损失在心脏病中起着至关重要的作用。自噬是一种进化保守的细胞分解代谢过程，通过该过程，长寿的蛋白质和受损的细胞器被靶向溶酶体降解。自噬对于心脏稳态很重要，可以通过提供能量来源作为一种保护机制，特别是在面临持续饥饿的情况下。细胞代谢与细胞存活密切相关，最近的证据表明代谢和自噬信号通路表现出高度的串扰并且在功能上相互依赖。在这篇综述中，我们讨论了在理解自噬调节及其与代谢信号传导的串扰方面的最新进展，重点关注营养感应 mTOR 复合物 1 (mTORC1) 通路。
The ability of adult cardiomyocytes to regenerate is limited, and irreversible loss by cell death plays a crucial role in heart diseases. Autophagy is an evolutionary conserved cellular catabolic process through which long-lived proteins and damaged organelles are targeted for lysosomal degradation. Autophagy is important in cardiac homeostasis and can serve as a protective mechanism by providing an energy source, especially in the face of sustained starvation. Cellular metabolism is closely associated with cell survival, and recent evidence suggests that metabolic and autophagic signaling pathways exhibit a high degree of crosstalk and are functionally interdependent. In this review, we discuss recent progress in our understanding of regulation of autophagy and its crosstalk with metabolic signaling, with a focus on the nutrient-sensing mTOR complex1 (mTORC1) pathway.