Yu Wen-wen, Bao Xiu-qi, Sun Hua, Zhang Dan
Yao Xue Xue Bao. 2015 Aug;50(8):945-50.
Neurodegenerative disease is characterized by progressive loss of neurons in specific brain regions that results in neuronal dysfunction of the central nervous system. Although the pathological mechanism is not fully established, the activation of glial cells mediated neuroinflammation appears to be involved. Heat shock protein 70 (HSP70) is originally described as intracellular chaperone, which plays an important role in protein quality control in cells. However, recent study showed that up-regulation of HSP70 had anti-inflammatory effects in the brain. HSP70 protected neurons from damage and improved neurological function by decreasing inflammatory response as indicated by inactivation of glial cells and inhibition of pro-inflammatory cytokine release. So it is of great significance to find new compounds targeting at HSP70 as neuroprotective agents to delay the progress of neurodegenerative disease. This review will focus on the role of HSP70 in neuroinflammation and the recent advances in using HSP70 as a target for the treatment of neurodegenerative disease.
神经退行性疾病的特征是特定脑区的神经元进行性丧失，导致中枢神经系统的神经元功能障碍。尽管其病理机制尚未完全明确，但胶质细胞介导的神经炎症激活似乎与之有关。热休克蛋白70（HSP70）最初被描述为细胞内伴侣蛋白，在细胞内蛋白质质量控制中发挥重要作用。然而，最近的研究表明，HSP70的上调在大脑中具有抗炎作用。HSP70通过减少炎症反应来保护神经元免受损伤并改善神经功能，这表现为胶质细胞失活和促炎细胞因子释放受到抑制。因此，寻找靶向HSP70的新化合物作为神经保护剂以延缓神经退行性疾病的进展具有重要意义。本综述将聚焦于HSP70在神经炎症中的作用以及将HSP70作为神经退行性疾病治疗靶点的最新进展。
