Gao Xiao-Yan, Yang Tuo, Gu Ying, Sun Xiao-Hong
Department of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, China.
Science Experiment Center, China Medical University, Shenyang, China.
Front Aging Neurosci. 2022 Jun 20;14:885500. doi: 10.3389/fnagi.2022.885500. eCollection 2022.
Parkinson's disease (PD) is one of the most common neurodegenerative movement disorders worldwide. There are currently no cures or preventative treatments for PD. Emerging evidence indicates that mitochondrial dysfunction is closely associated with pathogenesis of sporadic and familial PD. Because dopaminergic neurons have high energy demand, cells affected by PD exhibit mitochondrial dysfunction that promotes the disease-defining the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The mitochondrion has a particularly important role as the cellular "powerhouse" of dopaminergic neurons. Therefore, mitochondria have become a promising therapeutic target for PD treatments. This review aims to describe mitochondrial dysfunction in the pathology of PD, outline the genes associated with familial PD and the factors related to sporadic PD, summarize current knowledge on mitochondrial quality control in PD, and give an overview of therapeutic strategies for targeting mitochondria in neuroprotective interventions in PD.
帕金森病（PD）是全球最常见的神经退行性运动障碍之一。目前尚无针对帕金森病的治愈方法或预防性治疗措施。新出现的证据表明，线粒体功能障碍与散发性和家族性帕金森病的发病机制密切相关。由于多巴胺能神经元对能量需求较高，受帕金森病影响的细胞表现出线粒体功能障碍，进而促进疾病发展——这表现为黑质致密部（SNpc）中多巴胺能神经元的丧失。线粒体作为多巴胺能神经元的细胞“动力源”具有尤为重要的作用。因此，线粒体已成为帕金森病治疗的一个有前景的治疗靶点。本综述旨在描述帕金森病病理学中的线粒体功能障碍，概述与家族性帕金森病相关的基因以及与散发性帕金森病相关的因素，总结目前关于帕金森病中线粒体质量控制的知识，并概述在帕金森病神经保护干预中针对线粒体的治疗策略。
