The cell on the edge of life and death: Crosstalk between autophagy and apoptosis
The cell on the edge of life and death: Crosstalk between autophagy and apoptosis
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DOI：
10.5604/01.3001.0010.4672
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发表时间：
2017-09-21
影响因子：
0.3
通讯作者：
Kasprowska-Liskiewicz, Daniela
中科院分区：
文献类型：
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作者：
Kasprowska-Liskiewicz, Daniela
近年来，自噬和细胞凋亡之间的相互作用引起了更广泛的关注。基础自噬用于维持细胞稳态，而该过程的上调是应激反应的一个要素，使细胞能够在不利条件下生存。自噬还可以通过其与细胞死亡途径的相互作用来决定细胞的命运。控制这两个过程的启动和执行阶段的蛋白质网络是高度互连的。自噬和细胞凋亡之间存在多种相互影响的情况。在大多数情况下，自噬的激活代表细胞尝试应对应激，并保护细胞免于凋亡或延迟其启动。一般来说，自噬和凋亡之间的相互抑制串扰会阻止促生存和促死亡途径的同时激活。但在某些情况下，自噬或核心自噬机制的蛋白质可能通过过度的自我消化（所谓的“自噬细胞死亡”）或刺激其他细胞死亡途径的激活来促进细胞死亡。细胞是否真的通过自噬死亡存在争议，这就是为什么“自噬细胞死亡”一词最近引起了激烈的争论。本文综述了自噬与细胞凋亡之间多层次串扰的最新研究成果，包括共同调节因子、这些过程的相互抑制、自噬或自噬蛋白刺激细胞凋亡以及自噬作为死亡执行机制的作用。
Recently, the crosstalk between autophagy and apoptosis has attracted broader attention. Basal autophagy serves to maintain cell homeostasis, while the upregulation of this process is an element of stress response that enables the cell to survive under adverse conditions. Autophagy may also determine the fate of the cell through its interactions with cell death pathways. The protein networks that control the initiation and the execution phase of these two processes are highly interconnected. Several scenarios for the crosstalk between autophagy and apoptosis exist. In most cases, the activation of autophagy represents an attempt of the cell to cope with stress, and protects the cell from apoptosis or delays its initiation. Generally, the simultaneous activation of pro-survival and pro-death pathways is prevented by the mutual inhibitory crosstalk between autophagy and apoptosis. But in some circumstances, autophagy or the proteins of the core autophagic machinery may promote cellular demise through excessive self-digestion (so-called "autophagic cell death") or by stimulating the activation of other cell death pathways. It is controversial whether cells actually die via autophagy, which is why the term "autophagic cell death" has been under intense debate lately. This review summarizes the recent findings on the multilevel crosstalk between autophagy and apoptosis in aspects of common regulators, mutual inhibition of these processes, the stimulation of apoptosis by autophagy or autophagic proteins and finally the role of autophagy as a death-execution mechanism.