内质网应激可能是子痫前期发病机制之一。
Endoplasmic reticulum stress may be one of the mechanisms for PE development.
内质网应激是内质网内未折叠或错误折叠蛋白积聚所致。
Endoplasmic reticulum (ER) stress results from the accumulation of unfolded or misfolded proteins in the ER.
目的探讨内质网应激在高脂血症引起的肾脏损害中的作用。
Objective To investigate the effect of endoplasmic reticulum stress in renal damage caused by hyperlipidemia.
文章对脑缺血再灌注诱导内质网应激和upr的研究进展做了综述。
This article reviews the recent progress in er stress and UPR induced by cerebral ischemic-reperfusion.
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.
内质网应激很可能是IETM促进肝纤维化乃至肝硬化发生的重要机制。
Endoplasmic reticulum stress is a possible mechanism in the development of liver cirrhosis promoted by IETM.
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.
脂联素可以通过减轻内质网应激来减轻心肌细胞凋亡，对心肌细胞有保护作用。
Adiponectin decreases the endoplasmic reticulum stress injury and plays a protective role by extenuation of cadiomyocyte apoptosis.
结论：内质网应激介导的凋亡与大鼠慢性低氧性肺动脉高压、肺血管改建的病理过程有关。
Conclusion: the endoplasmic reticulum stress-induced apoptosis may be one of the mechanism of hypoxic pulmonary hypertension and pulmonary vascular wall remodeling.
这可能与脊髓损伤后海马和皮质区域发生的内质网应激引起海马与皮质区域神经细胞受损有关。
It may be related to the impairment of the hippocampus and cortical areas in the hippocampus and cortex induced by endoplasmic reticulum stress after spinal cord injury.
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.
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.
NAFLD发病机制尚不明确，胰岛素抵抗、氧化应激、 代谢紊乱、脂肪因子、内质网应激可能发挥重要作用。
The pathogenesy of this disease is not clear, and insulin resistance, oxidative stress, adipokins and endoplasmic re…
目的：观察高糖慢性处理对血管内皮细胞内质网应激标志蛋白葡萄糖调节蛋白78 (GRP78)表达的影响及其作用机制。
AIM: To investigate the effect of high glucose on the expression of an endoplasmic reticulum stress marker glucose-regulated protein 78 (GRP78), and explore its underlying mechanism.
有研究证实内质网应激能影响软骨细胞的分化，同时也抑制了软骨细胞的合成功能，减少异常蛋白的合成，减轻应激对细胞的损害。
It has been proved that ERS can interfere the differentiation of chondrocyte, decrease the synthesis of abnormal protein, attenuate the injury of cell.
结论：PC对脑缺血再灌注损伤大鼠具有保护作用，其机制可能与其增加GRP78表达、拮抗chop表达、阻断内质网应激(ERS)启动的凋亡通路有关。
Conclusion: PC has a protective effect on cerebral IR injury, which may related to increased GRP78 and decreased CHOP expression, and to inhibition of the ERS-induced apoptosis pathway.
他们的发现支持这样的观点，即所谓的内质网（ER）应激性与机体自然处理的方式是一致的，该方式是破裂发生的一个原因。
Their finding supports the idea that so-called endoplasmic reticulum (ER) stress together with the body's natural way of coping with that stress is one reason why the rupture takes place.
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.
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.
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