The Endoplasmic Reticulum Stress/Unfolded Protein Response and Their Contributions to Parkinson's Disease Physiopathology.
The Endoplasmic Reticulum Stress/Unfolded Protein Response and Their Contributions to Parkinson's Disease Physiopathology.
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内质网应激/未折叠蛋白反应及其对帕金森病生理病理学的贡献
DOI：
10.3390/cells9112495
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发表时间：
2020-11-17
期刊：
影响因子：
6
通讯作者：
Checler F
中科院分区：
文献类型：
--
作者：
Costa CAD;Manaa WE;Duplan E;Checler F
帕金森病(PD)是一种与年龄相关的多因素运动障碍，已有线粒体和内质网(ER)缺陷的报道。未折叠蛋白反应(UPR)已成为一种与疾病病因相关的关键细胞功能障碍。UPR涉及内质网启动的协调反应，从而实现蛋白质的正确折叠。本文就内质网及其功能、UPR信号转导通路以及内质网应激、UPR激活与帕金森病生理病理之间的关系作一综述。因此，描述了通过体外和体内药理学方法或通过帕金森病致病基因的遗传调节获得的死后研究和数据。此外，我们还讨论了UPR与散发性和遗传性帕金森病的相关性和影响。
Parkinson’s disease (PD) is a multifactorial age-related movement disorder in which defects of both mitochondria and the endoplasmic reticulum (ER) have been reported. The unfolded protein response (UPR) has emerged as a key cellular dysfunction associated with the etiology of the disease. The UPR involves a coordinated response initiated in the endoplasmic reticulum that grants the correct folding of proteins. This review gives insights on the ER and its functioning; the UPR signaling cascades; and the link between ER stress, UPR activation, and physiopathology of PD. Thus, post-mortem studies and data obtained by either in vitro and in vivo pharmacological approaches or by genetic modulation of PD causative genes are described. Further, we discuss the relevance and impact of the UPR to sporadic and genetic PD pathology.
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影响因子：
7.2
作者：
Braakman, Ineke;Hebert, Daniel N.
通讯作者：
Hebert, Daniel N.
影响因子：
4
作者：
Berridge, MJ
通讯作者：
Berridge, MJ
影响因子：
3.5
作者：
Chinta, Shankar J.;Rane, Anand;Poksay, Karen S.;Bredesen, Dale E.;Andersen, Julie K.;Rao, Rammohan V.
通讯作者：
Rao, Rammohan V.
DOI：
10.1523/jneurosci.5367-11.2012
发表时间：
2012-03-07
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Colla E;Coune P;Liu Y;Pletnikova O;Troncoso JC;Iwatsubo T;Schneider BL;Lee MK
通讯作者：
Lee MK
DOI：
10.1073/pnas.96.20.11041
发表时间：
1999-09-28
影响因子：
11.1
作者：
Brown, MS;Goldstein, JL
通讯作者：
Goldstein, JL