期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/ijms21093369
关键词
autophagy; neurodegenerative disease; protein aggregates
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science and ICT [MRC 2014R1A5A2009392]
- Ministry of Education [2016R1A6A3A04006478, 2019S1A5C2A03082727]
- National Research Foundation of Korea [2019S1A5C2A03082727] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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 beta and alpha-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.
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