Autophagy in Neurodegenerative Diseases: A Hunter for Aggregates

Cells have developed elaborate quality-control mechanisms for proteins and organelles to maintain cellular homeostasis. Such quality-control mechanisms are maintained by conformational folding via molecular chaperones and by degradation through the ubiquitin-proteasome or autophagy-lysosome system....

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Main Authors: Hyungsun Park, Ju-Hee Kang, Seongju Lee
Format: Article
Language:English
Published: MDPI AG 2020-05-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/21/9/3369
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spelling doaj-084068fa200c47c598a344497129c3e42020-11-25T02:41:49ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-05-01213369336910.3390/ijms21093369Autophagy in Neurodegenerative Diseases: A Hunter for AggregatesHyungsun Park0Ju-Hee Kang1Seongju Lee2Department of Anatomy, College of Medicine, Inha University, Incheon 22212, KoreaHypoxia-related Disease Research Center, College of Medicine, Inha University, Incheon 22212, KoreaDepartment of Anatomy, College of Medicine, Inha University, Incheon 22212, KoreaCells have developed elaborate quality-control mechanisms for proteins and organelles to maintain cellular homeostasis. Such quality-control mechanisms are maintained by conformational folding via molecular chaperones and by degradation through the ubiquitin-proteasome or autophagy-lysosome system. Accumulating evidence suggests that impaired autophagy contributes to the accumulation of intracellular inclusion bodies consisting of misfolded proteins, which is a hallmark of most neurodegenerative diseases. In addition, genetic mutations in core autophagy-related genes have been reported to be linked to neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. Conversely, the pathogenic proteins, such as amyloid β and α-synuclein, are detrimental to the autophagy pathway. Here, we review the recent advances in understanding the relationship between autophagic defects and the pathogenesis of neurodegenerative diseases and suggest autophagy induction as a promising strategy for the treatment of these conditions.https://www.mdpi.com/1422-0067/21/9/3369autophagyneurodegenerative diseaseprotein aggregates
collection DOAJ
language English
format Article
sources DOAJ
author Hyungsun Park
Ju-Hee Kang
Seongju Lee
spellingShingle Hyungsun Park
Ju-Hee Kang
Seongju Lee
Autophagy in Neurodegenerative Diseases: A Hunter for Aggregates
International Journal of Molecular Sciences
autophagy
neurodegenerative disease
protein aggregates
author_facet Hyungsun Park
Ju-Hee Kang
Seongju Lee
author_sort Hyungsun Park
title Autophagy in Neurodegenerative Diseases: A Hunter for Aggregates
title_short Autophagy in Neurodegenerative Diseases: A Hunter for Aggregates
title_full Autophagy in Neurodegenerative Diseases: A Hunter for Aggregates
title_fullStr Autophagy in Neurodegenerative Diseases: A Hunter for Aggregates
title_full_unstemmed Autophagy in Neurodegenerative Diseases: A Hunter for Aggregates
title_sort autophagy in neurodegenerative diseases: a hunter for aggregates
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1661-6596
1422-0067
publishDate 2020-05-01
description Cells have developed elaborate quality-control mechanisms for proteins and organelles to maintain cellular homeostasis. Such quality-control mechanisms are maintained by conformational folding via molecular chaperones and by degradation through the ubiquitin-proteasome or autophagy-lysosome system. Accumulating evidence suggests that impaired autophagy contributes to the accumulation of intracellular inclusion bodies consisting of misfolded proteins, which is a hallmark of most neurodegenerative diseases. In addition, genetic mutations in core autophagy-related genes have been reported to be linked to neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. Conversely, the pathogenic proteins, such as amyloid β and α-synuclein, are detrimental to the autophagy pathway. Here, we review the recent advances in understanding the relationship between autophagic defects and the pathogenesis of neurodegenerative diseases and suggest autophagy induction as a promising strategy for the treatment of these conditions.
topic autophagy
neurodegenerative disease
protein aggregates
url https://www.mdpi.com/1422-0067/21/9/3369
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AT juheekang autophagyinneurodegenerativediseasesahunterforaggregates
AT seongjulee autophagyinneurodegenerativediseasesahunterforaggregates
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