摘要
阿尔茨海默病的发病机理的特征是β淀粉Aβ(1-42)毒性片段聚合及与之相关的受损自噬。在线粒体中,由酶催化过程与活性氧(ROS)产生而引起慢性损伤,随后Aβ以老年斑的形式积累和细胞内沉积物的过度磷酸化tau蛋白的积累被称为纤维缠结。蛋白酶激活受体(PARs)是G蛋白偶合受体(GPCR)家族的成员,能促进和调节各种亚细胞分子成分的跨细胞运输和分配到溶酶体系统。因此,能够影响他们的降解。数据表明,PARs的激活或抑制引起自噬过程的变化,这可能影响ROS的产生和Aβ(1-42)降解溶酶体并导致AD发病。
关键词: β淀粉样蛋白,阿尔茨海默病,自体吞噬,蛋白tau,蛋白酶活化受体,活性氧。
Current Alzheimer Research
Title:The Contribution of Proteinase-Activated Receptors to Intracellular Signaling, Transcellular Transport and Autophagy in Alzheimer´s Disease
Volume: 12 Issue: 1
Author(s): Radoslav Matej, Zdenek Rohan, Karel Holada and Tomas Olejar
Affiliation:
关键词: β淀粉样蛋白,阿尔茨海默病,自体吞噬,蛋白tau,蛋白酶活化受体,活性氧。
摘要: The etiopathogenesis of Alzheimer´s disease is characterized by beta amyloid Aβ(1-42) toxic fragment aggregation and its association with impaired autophagy. In mitochondria, chronic damage due to transport and enzymatic processes together with the production of reactive oxygen species (ROS) are followed by the subsequent accumulation of Aβ in the form of senile plaques and the accumulation of hyperphosphorylated tau protein in intracellular deposits called tangles. Proteinase-activated receptors (PARs), members of the G protein-coupled receptor (GPCR) family, facilitate and modulate the transcellular transport and distribution of a variety of subcellular molecular components to the lysosomal system and, thus, influence their degradation. A review of the data shows that the activation or inhibition of PARs leads to changes in the process of autophagy, which may influence ROS production and Aβ (1-42) degradation in lysosomes and result in AD pathogenesis.
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Cite this article as:
Matej Radoslav, Rohan Zdenek, Holada Karel and Olejar Tomas, The Contribution of Proteinase-Activated Receptors to Intracellular Signaling, Transcellular Transport and Autophagy in Alzheimer´s Disease, Current Alzheimer Research 2015; 12 (1) . https://dx.doi.org/10.2174/1567205012666141218123202
DOI https://dx.doi.org/10.2174/1567205012666141218123202 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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