PINK1 and Parkin to control mitochondria remodeling.
PINK1 and Parkin to control mitochondria remodeling.
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DOI：
10.5115/acb.2010.43.3.179
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发表时间：
2010-09
影响因子：
1.1
通讯作者：
Chung J
中科院分区：
文献类型：
--
作者：
Koh H;Chung J
帕金森病（PD）是最常见的神经退行性疾病之一，其特征是运动障碍和多巴胺能（DA）神经元的丧失。PD主要是偶发的，但也可能是由一些PD相关基因的基因突变引起的。最近，对果蝇突变体parkin和PINK1这两个常见的pd相关基因的遗传学研究表明，parkin在PINK1的下游发挥作用，维持线粒体功能和完整性。进一步的研究表明，PINK1将Parkin易位到线粒体并调节关键的线粒体重塑过程。这些发现表明，线粒体功能障碍是帕金森病发病的一个重要原因，为帕金森病的有效治疗提供了有价值的见解。
Parkinson's disease (PD), one of the most common neurodegenerative diseases, is characterized by movement disorders and a loss of dopaminergic (DA) neurons. PD mainly occurs sporadically, but may also result from genetic mutations in several PD-linked genes. Recently, genetic studies with Drosophila mutants, parkin and PINK1, two common PD-associated genes, demonstrated that Parkin acts downstream of PINK1 in maintaining mitochondrial function and integrity. Further studies revealed that PINK1 translocates Parkin to mitochondria and regulates critical mitochondrial remodeling processes. These findings, which suggest that mitochondrial dysfunction is a prominent cause of PD pathogenesis, provide valuable insights which may aid in the development of effective treatments for PD.