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帕金森病发病机制至今未明,近几年研究发现,线粒体依赖性PCD通路的激活在PD发病过程中是不可缺少的,不同形态学表现的细胞死亡形式在帕金森病发病过程中可以共同存在,而所有的这些细胞死亡都归因于PCD共同的上游通路的激活。PCD通路不仅仅是指线粒体介导的caspase依赖性凋亡,还包括非caspase依赖性细胞非凋亡性死亡,比如细胞坏死。这不仅仅是概念上的延伸,更为我们在帕金森病神经保护性治疗上提供了更多的靶点,有助于寻求神经保护的新方法和延缓神经退行性疾病的进程.抗凋亡治疗已经成为帕金森病等神经退行性疾病治疗的新热点,已经证实,caspase抑制剂能够通过抑制caspase的激活,阻止细胞退行性病变。那么将位于caspase执行者上游的Bax作为靶点,抑制Bax的激活与转位,能够产生更为持久显著的神经保护作用。本文综述了近年来相关研究进展。
The pathogenesis of Parkinson’s disease is still unknown. In recent years, it has been found that the activation of mitochondria-dependent PCD pathway is indispensable in the pathogenesis of PD. The cell death patterns of different morphological manifestations may co-exist in the pathogenesis of Parkinson’s disease. All of these cell deaths are attributed to the activation of the PCD common upstream pathway. The PCD pathway not only refers to mitochondria-mediated caspase-dependent apoptosis, but also non-caspase dependent non-apoptotic deaths, such as necrosis. This is not just a conceptual extension, but it also provides us more targets for neuroprotective treatment of Parkinson’s disease, helps to find new ways of neuroprotection and delays the progression of neurodegenerative diseases. Treatment has become a new hot spot in the treatment of neurodegenerative diseases such as Parkinson’s disease. It has been confirmed that caspase inhibitors can prevent cell degenerative diseases by inhibiting caspase activation. Then targeting Bax upstream of caspase executors and inhibiting the activation and translocation of Bax can produce more sustained and significant neuroprotection. This article summarizes the recent research progress.