ER Stress-Mediated Signaling: Action Potential and Ca(2+) as Key Players.

ER Stress-Mediated Signaling: Action Potential and Ca(2+) as Key Players.
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DOI:
10.3390/ijms17091558
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发表时间:
2016-09-15
影响因子:
5.6
通讯作者:
Yoon H
Yoon H
中科院分区:
生物学2区
文献类型:
--
作者:
Bahar E;Kim H;Yoon H

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内质网 (ER) 的正常功能对于多种细胞活动和生存至关重要。正常内质网功能的紊乱会导致未折叠蛋白的积累和聚集,从而启动适应性反应,即未折叠蛋白反应(UPR),以恢复正常的内质网功能。未能激活适应性反应会启动程序性细胞死亡或细胞凋亡的过程。细胞凋亡在细胞消除中发挥重要作用,这对于胚胎发生、发育和组织稳态至关重要。细胞凋亡受损可导致各种病理状况的发展,例如神经退行性疾病和自身免疫性疾病、癌症或获得性免疫缺陷综合症(艾滋病)。钙 (Ca2+) 是细胞存活的关键调节剂之一,它可以响应各种条件诱导内质网应激介导的细胞凋亡。 Ca2+ 在细胞凋亡的早期和晚期调节细胞死亡。严重的 Ca2+ 失调可通过细胞凋亡促进细胞死亡。动作电位是一种沿着神经元和肌肉纤维传输的电信号,对于向大脑、从大脑以及在大脑内传递信息非常重要。动作电位启动后,胞质 Ca2+ 水平升高(去极化)导致内质网应激反应激活,从而引发细胞凋亡。在这篇综述中,我们讨论了 Ca2+ 和动作电位在内质网应激介导的细胞凋亡中的作用。
The proper functioning of the endoplasmic reticulum (ER) is crucial for multiple cellular activities and survival. Disturbances in the normal ER functions lead to the accumulation and aggregation of unfolded proteins, which initiates an adaptive response, the unfolded protein response (UPR), in order to regain normal ER functions. Failure to activate the adaptive response initiates the process of programmed cell death or apoptosis. Apoptosis plays an important role in cell elimination, which is essential for embryogenesis, development, and tissue homeostasis. Impaired apoptosis can lead to the development of various pathological conditions, such as neurodegenerative and autoimmune diseases, cancer, or acquired immune deficiency syndrome (AIDS). Calcium (Ca2+) is one of the key regulators of cell survival and it can induce ER stress-mediated apoptosis in response to various conditions. Ca2+ regulates cell death both at the early and late stages of apoptosis. Severe Ca2+ dysregulation can promote cell death through apoptosis. Action potential, an electrical signal transmitted along the neurons and muscle fibers, is important for conveying information to, from, and within the brain. Upon the initiation of the action potential, increased levels of cytosolic Ca2+ (depolarization) lead to the activation of the ER stress response involved in the initiation of apoptosis. In this review, we discuss the involvement of Ca2+ and action potential in ER stress-mediated apoptosis.
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