目的：探讨内质网应激反应对于诱导病毒性心肌炎心肌细胞凋亡的作用。
Objective: to investigate the role of endoplasmic reticulum stress in induction of cardiac myocyte apoptosis in viral myocarditis.
结论：内质网应激反应可能对于诱导病毒性心肌炎的心肌细胞凋亡有一定作用。
Conclusion: These findings suggest endoplasmic reticulum stress may contribute to the cardiac myocyte apoptosis in viral myocarditis.
近年来在凋亡机制的研究中发现内质网应激反应介导的细胞凋亡是一条新的细胞凋亡信号传导通路。
In recent years, the study found that the apoptosis mechanism of endoplasmic reticulum stress-mediated apoptosis is a new signaling pathway of apoptosis.
作为对内质网应激的响应，细胞形成了一条称为未折叠蛋白反应(upr)的自我保护信号转导通路。
In response to er stress, cells have developed a self-protective signal transduction pathway termed the unfolded protein response (UPR).
内质网中钙离子紊乱和未折叠蛋白质蓄积，可引发内质网应激，发生具有保护作用的未折叠蛋白反应。
The disorder of calcium iron and accumulation of unfolded protein can lead to er stress and thus protective unfolded protein response ensure.
细胞对这种应激的反应是增加一系列内质网分子伴侣如GRP94、GRP78和PDI等的表达。
Normal cells respond to ER stress by increasing transcription of genes encoding ER-resident molecular chaperones such as GRP94, GRP78 and PDI to facilitate protein folding.
但是反应功能障碍或者过强、过长时间的内质网应激都可以引起细胞功能失调，甚至细胞死亡。
However, the heavy and continued endoplasmic reticulum stress can lead to cell dysfunction and even cell death.
但是反应功能障碍或者过强、过长时间的内质网应激都可以引起细胞功能失调，甚至细胞死亡。
However, the heavy and continued endoplasmic reticulum stress can lead to cell dysfunction and even cell death.
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