کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8478693 | 1551150 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mitophagy and Parkinson's disease: Be eaten to stay healthy
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کلمات کلیدی
PINK1(PD)Mitochondrial DNA - DNA میتوکندریاAutophagy - اتوفاژیParkinson's disease - بیماری پارکینسونsubstantia nigra pars compacta - توده سیاه پارس متراکمmitochondrial outer membrane - غشای بیرونی میتوکندریMitophagy - میتوفاژیMitochondria - میتوکندریاParkin - پارکینMitochondrial membrane potential - پتانسیل غشای میتوکندریcarbonyl cyanide m-chlorophenylhydrazone - کربنیل سیانید m-chlorophenylhydrazone
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Parkinson's disease (PD) is one of the most prevalent neurodegenerative disorders. Pathologically, it is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNc). Although most occurrences have an unknown cause, several gene mutations have been linked to familial forms of PD. The discovery of some of the proteins encoded by these genes, including Parkin, PINK1 and DJ-1, at the mitochondria offered a new perspective on the involvement of mitochondria in PD. Specifically, these proteins are thought to be involved in the maintenance of a healthy pool of mitochondria by regulating their turnover by mitochondrial autophagy, or mitophagy. In this review, we discuss recent studies on the role of mitophagy in PD. We present three putative models whereby PINK1 and Parkin may affect mitophagy; 1) by shifting the balance between fusion and fission of the mitochondrial network, 2) by modulating mitochondrial motility and 3) by directly recruiting the autophagic machinery to damaged mitochondria. This article is part of a Special Issue entitled 'Mitochondrial function and dysfunction in neurodegeneration'.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 55, July 2013, Pages 37-43
Journal: Molecular and Cellular Neuroscience - Volume 55, July 2013, Pages 37-43
نویسندگان
Rosa L.A. de Vries, Serge Przedborski,