Regulation of autophagy by metabolic and stress signaling pathways in the heart.
Regulation of autophagy by metabolic and stress signaling pathways in the heart.
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DOI：
10.1097/fjc.0b013e318256cdd0
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发表时间：
2012-08
影响因子：
3
通讯作者：
Gustafsson AB
中科院分区：
文献类型：
--
作者：
Lee Y;Lee HY;Gustafsson AB
自噬是在正常和应激条件下维持心脏细胞内稳态的重要过程。自噬是一个关键的降解途径，并作为一个质量控制传感器。它通过快速清除细胞内的细胞毒性蛋白质聚集体和功能失调的细胞器来保护肌细胞。它还对能量需求和机械压力的变化做出反应，以维持收缩功能。自噬-溶酶体途径对血清饥饿作出反应，以确保细胞在营养不足时维持其代谢和能量水平。相反，自噬的过度激活对细胞是有害的，并有助于病理条件的发展。许多信号通路和蛋白质调节自噬。这些包括AMPK/mTOR通路、FoxO转录因子、Sirt 1、氧化应激、Bcl-2家族蛋白和E3泛素连接酶Parkin。在这篇综述中，我们将讨论如何不同演员的字符调节重要的自噬过程中的心肌。
Autophagy is an essential process for the maintenance of cellular homeostasis in the heart under both normal and stress conditions. Autophagy is a key degradation pathway and acts as a quality control sensor. It protects myocytes from cytotoxic protein aggregates and dysfunctional organelles by quickly clearing them from cell. It also responds to changes in energy demand and mechanical stressors to maintain contractile function. The autophagic-lysosomal pathway responds to serum starvation to ensure that the cell maintains its metabolism and energy levels when nutrients run low. In contrast, excessive activation of autophagy is detrimental to cells and contributes to development of pathological conditions. A number of signaling pathways and proteins regulate autophagy. These include the AMPK/mTOR pathway, FoxO transcription factors, Sirt1, oxidative stress, Bcl-2 family proteins, and the E3 ubiquitin ligase Parkin. In this review, we will discuss how this diverse cast of characters regulates the important autophagic process in the myocardium.