Tan Valerie P, Miyamoto Shigeki
Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0636, USA.
Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0636, USA.
J Mol Cell Cardiol. 2016 Jun;95:31-41. doi: 10.1016/j.yjmcc.2016.01.005. Epub 2016 Jan 7.
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 evolutionarily 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 complex 1 (mTORC1) pathway.
成人心肌细胞的再生能力有限，细胞死亡导致的不可逆损失在心脏疾病中起关键作用。自噬是一种进化上保守的细胞分解代谢过程，通过该过程，长寿命蛋白质和受损细胞器被靶向进行溶酶体降解。自噬在心脏内环境稳态中很重要，并且可以通过提供能量来源充当一种保护机制，尤其是在持续饥饿的情况下。细胞代谢与细胞存活密切相关，最近的证据表明，代谢信号通路和自噬信号通路表现出高度的相互作用且在功能上相互依存。在本综述中，我们讨论了在自噬调控及其与代谢信号相互作用方面的最新进展，重点是营养感应的mTOR复合体1（mTORC1）途径。
