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帕金森病中的线粒体功能障碍:发病机制与神经保护。

Mitochondrial dysfunction in Parkinson's disease: pathogenesis and neuroprotection.

机构信息

School of Medical Sciences, College of Life Sciences and Medicine, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UK.

出版信息

Parkinsons Dis. 2010 Dec 26;2011:617472. doi: 10.4061/2011/617472.

DOI:10.4061/2011/617472
PMID:21234411
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3014704/
Abstract

Mitochondria are vitally important organelles involved in an array of functions. The most notable is their prominent role in energy metabolism, where they generate over 90% of our cellular energy in the form of ATP through oxidative phosphorylation. Mitochondria are involved in various other processes including the regulation of calcium homeostasis and stress response. Mitochondrial complex I impairment and subsequent oxidative stress have been identified as modulators of cell death in experimental models of Parkinson's disease (PD). Identification of specific genes which are involved in the rare familial forms of PD has further augmented the understanding and elevated the role mitochondrial dysfunction is thought to have in disease pathogenesis. This paper provides a review of the role mitochondria may play in idiopathic PD through the study of experimental models and how genetic mutations influence mitochondrial activity. Recent attempts at providing neuroprotection by targeting mitochondria are described and their progress assessed.

摘要

线粒体是参与多种功能的重要细胞器。它们最显著的作用是在能量代谢中,通过氧化磷酸化产生超过 90%的细胞能量形式的 ATP。线粒体还参与其他各种过程,包括钙稳态的调节和应激反应。线粒体复合物 I 损伤和随后的氧化应激已被确定为帕金森病 (PD) 实验模型中细胞死亡的调节剂。鉴定参与罕见家族性 PD 的特定基因进一步增强了对线粒体功能障碍在疾病发病机制中作用的理解。本文通过研究实验模型,综述了线粒体在特发性 PD 中可能发挥的作用,以及遗传突变如何影响线粒体活性。描述了最近通过靶向线粒体提供神经保护的尝试,并评估了它们的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22ab/3014704/cc16b5f135a8/PD2011-617472.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22ab/3014704/f38a36f34dd0/PD2011-617472.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22ab/3014704/cc16b5f135a8/PD2011-617472.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22ab/3014704/f38a36f34dd0/PD2011-617472.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/22ab/3014704/cc16b5f135a8/PD2011-617472.002.jpg

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