期刊
INTERNATIONAL JOURNAL OF NEUROSCIENCE
卷 122, 期 12, 页码 695-703出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/00207454.2012.714430
关键词
amyotrophic lateral sclerosis; autophagic flux; autophagy; SOD1; TDP-43
资金
- Major State Basic Research Development Program of China (973 Program) [2011CB510000]
- National 863 High-Tech Research and Development Program of China [2006AA02A408]
- National Natural Science Foundation of China [30570638, 30770735, 30971035, 30900469]
Autophagy is a degradative modality that involves intracellular elimination of proteins and organelles by lysosomes. It is a conservative process and plays a crucial role in cell growth and development, and keeping cellular homeostasis especially under stress-induced situations. Recently, increasing evidence suggests that autophagic alternations may contribute to amyotrophic lateral sclerosis (ALS) as one of initial factors. LC3-II and p62 are found increased in spinal cord of both ALS patients and experimental models, indicating overwhelming autophagic level. But the aggregation of ALS-associated proteins, including SOD1 and TDP-43 suggest possible insufficiency of autophagy induction. Besides, augment autophagic level through genetic pathway or rapamycin leads to paradoxical results in different neurodegenerative diseases models. So, it remains controversial about autophagic effects on ALS progress. In this review, we will depict a comprehensive role that autophagy plays in ALS and focus on the influence of impaired autophagic flux and excessive autophagic vacuoles (AVs) that may aggregate ALS development. And we will discuss the potential therapeutic targets through modulating autophagic level to treat this disease.
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