自噬
mTORC1型
串扰
细胞生物学
营养感应
生物
PI3K/AKT/mTOR通路
代谢途径
溶酶体
分解代谢
程序性细胞死亡
信号转导
细胞器
新陈代谢
细胞凋亡
生物化学
酶
物理
光学
作者
Valerie Tan,Shigeki Miyamoto
标识
DOI:10.1016/j.yjmcc.2016.01.005
摘要
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.
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