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首页> 外文期刊>Journal of Cellular Physiology >Crosstalk of autophagy and apoptosis: Involvement of the dual role of autophagy under ER stress
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Crosstalk of autophagy and apoptosis: Involvement of the dual role of autophagy under ER stress

机译：自噬和凋亡的相声:参与自噬的双重角色下ER应激

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摘要

Endoplasmic reticulum ( ER) stress is a common cellular stress response that is triggered by a variety of conditions that disturb cellular homeostasis, and induces cell apoptosis. Autophagy, an important and evolutionarily conserved mechanism for maintaining cellular homeostasis, is closely related to the apoptosis induced by ER stress. There are common upstream signaling pathways between autophagy and apoptosis induced by ER stress, including PERK/ATF4, IRE1 alpha, ATF6, and Ca2+. Autophagy can not only block the induction of apoptosis by inhibiting the activation of apoptosis-associated caspase which could reduce cellular injury, but also help to induce apoptosis. In addition, the activation of apoptosis-related proteins can also inhibit autophagy by degrading autophagy-related proteins, such as Beclin-1, Atg4D, Atg3, and Atg5. Although the interactions of different autophagy-and apoptosis-related proteins, and also common upstream signaling pathways have been found, the potential regulatory mechanisms have not been clearly understood. In this review, we summarize the dual role of autophagy, and the interplay and potential regulatory mechanisms between autophagy and apoptosis under ER stress condition.
机译：压力是一种常见的内质网(ER)细胞应激反应引发的各种各样的干扰细胞的条件体内平衡,诱发细胞凋亡。自噬,一个重要的进化维持细胞的保护机制体内平衡,细胞凋亡密切相关ER应激引起的。信号通路与自噬ER应激诱导细胞凋亡,其中包括活跃/ ATF4 IRE1α,ATF6和Ca2 +。不仅可以阻止细胞凋亡的诱导抑制凋亡的激活半胱天冬酶从而减少细胞损伤,但是也有助于诱导细胞凋亡。激活apoptosis-related蛋白质也可以抑制自噬降解autophagy-related蛋白质,如Beclin-1 Atg4D Atg3,Atg5。autophagy-and apoptosis-related蛋白质,也常见的上游信号通路发现,潜在的监管机制没有清楚地理解。总结自噬的双重角色,相互作用和潜在的监管机制自噬与凋亡在ER应激条件。

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