期刊
NEUROLOGY RESEARCH INTERNATIONAL
卷 2012, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2012/878030
关键词
-
资金
- NIH [NS063202]
- UAMS
- Department of Neurobiology and Developmental Sciences, Center for translational Neurosciences
- National Center for Research Resources [5P20RR020146-09]
- National Institute of General Medical Sciences [8 P20 GM103425-09]
- COBRE
- Paul Dunn Fund
- Deutsche Forschungsgemeinschaft [Pe 924/2-2]
Nrf2 (nuclear erythroid 2-related factor 2) is a basic region leucine-zipper transcription factor which binds to the antioxidant response element (ARE) and thereby regulates the expression of a large battery of genes involved in the cellular antioxidant and anti-inflammatory defence as well as mitochondrial protection. As oxidative stress, inflammation and mitochondrial dysfunctions have been identified as important pathomechanisms in amyotrophic lateral sclerosis (ALS), this signaling cascade has gained interest both with respect to ALS pathogenesis and therapy. Nrf2 and Keap1 expressions are reduced in motor neurons in postmortem ALS tissue. Nrf2-activating compounds have shown therapeutic efficacy in the ALS mouse model and other neurodegenerative disease models. Alterations in Nrf2 and Keap1 expression and dysregulation of the Nrf2/ ARE signalling programcould contribute to the chronic motor neuron degeneration in ALS and other neurodegenerative diseases. Therefore, Nrf2 emerges as a key neuroprotective molecule in neurodegenerative diseases. Our recent studies strongly support that the Nrf2/ARE signalling pathway is an important mediator of neuroprotection and therefore represents a promising target for development of novel therapies against ALS, Parkinson's disease (PD), Huntington's disease (HD), and Alzheimer's disease (AD).
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据