Biomedical Neuroscience Institute (BNI), Faculty of Medicine, University of Chile, Santiago, Chile.
Center for Geroscience, Brain Health and Metabolism (GERO), Santiago, Chile.
Biol Cell. 2019 Jun;111(6):161-168. doi: 10.1111/boc.201800068. Epub 2019 Mar 25.
Parkinson's disease is the second most common neurodegenerative disorder, leading to the progressive decline of motor control due to the loss of dopaminergic neurons in the substantia nigra pars compacta. At the molecular level, Parkinson's disease share common molecular signatures with most neurodegenerative diseases including the accumulation of misfolded proteins in the brain. Alteration in the buffering capacity of the proteostasis network during aging is proposed as one of the triggering steps leading to abnormal protein aggregation in this disease, highlighting disturbances in the function of the endoplasmic reticulum (ER). The ER is the main subcellular compartment involved in protein folding and quality control. ER stress triggers a signalling reaction known as the unfolded protein response (UPR), which aims restoring proteostasis through the induction of adaptive programs or the activation of cell death pathways when damage is chronic and cannot be repaired. Here, we overview most evidence linking ER stress to Parkinson's disease. Strategies to alleviate ER stress by targeting specific components of the UPR using small molecules and gene therapy are highlighted.
帕金森病是第二常见的神经退行性疾病,由于黑质致密部多巴胺能神经元的丧失,导致运动控制逐渐下降。在分子水平上,帕金森病与大多数神经退行性疾病具有共同的分子特征,包括大脑中错误折叠蛋白质的积累。有人提出,衰老过程中蛋白质稳态网络缓冲能力的改变是导致这种疾病中异常蛋白质聚集的触发步骤之一,这突出了内质网 (ER) 功能的紊乱。内质网是参与蛋白质折叠和质量控制的主要亚细胞区室。内质网应激会引发一种称为未折叠蛋白反应 (UPR) 的信号反应,当损伤是慢性的且无法修复时,该反应旨在通过诱导适应性程序或激活细胞死亡途径来恢复蛋白质稳态。在这里,我们综述了将内质网应激与帕金森病联系起来的大多数证据。强调了使用小分子和基因治疗靶向 UPR 的特定成分来减轻内质网应激的策略。