期刊
ANTIOXIDANTS
卷 10, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/antiox10071011
关键词
glutathione; oxidative stress; amyotrophic lateral sclerosis; neurogenerative disease
资金
- National Research Foundation of Korea (NRF) - Ministry of Science and ICT (MSIT) [NRF-2017R1C1B1008825, NRF-2019R1F1A1045639]
- Soonchunhyang University Research Fund
ALS is a rare neurological disorder characterized by a deficiency in the antioxidant tripeptide glutathione (GSH). Imbalanced GSH homeostasis and its molecular characteristics play crucial roles in ALS development. Studies have shown that GSH metabolism and redox status are associated with neuronal toxicity in ALS.
Amyotrophic lateral sclerosis (ALS) is a rare neurological disorder that affects the motor neurons responsible for regulating muscle movement. However, the molecular pathogenic mechanisms of ALS remain poorly understood. A deficiency in the antioxidant tripeptide glutathione (GSH) in the nervous system appears to be involved in several neurodegenerative diseases characterized by the loss of neuronal cells. Impaired antioxidant defense systems, and the accumulation of oxidative damage due to increased dysfunction in GSH homeostasis are known to be involved in the development and progression of ALS. Aberrant GSH metabolism and redox status following oxidative damage are also associated with various cellular organelles, including the mitochondria and nucleus, and are crucial factors in neuronal toxicity induced by ALS. In this review, we provide an overview of the implications of imbalanced GSH homeostasis and its molecular characteristics in various experimental models of ALS.
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