期刊
REDOX BIOLOGY
卷 38, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.redox.2020.101803
关键词
Nrf2; Reactive oxygen species; Oxidative stress; Skeletal muscle; Hormesis; Duchenne muscular dystrophy
资金
- Victoria University
- University Children's Hospital Basel
This article discusses the theoretical background of targeting Nrf2 as a disease-modifying treatment for Duchenne Muscular Dystrophy, highlighting the potential of targeted Nrf2 activation to simultaneously modulate different pathological features of the disease to enhance therapeutic effectiveness.
Imbalances in redox homeostasis can result in oxidative stress, which is implicated in various pathological conditions including the fatal neuromuscular disease Duchenne Muscular Dystrophy (DMD). DMD is a complicated disease, with many druggable targets at the cellular and molecular level including calcium-mediated muscle degeneration; mitochondrial dysfunction; oxidative stress; inflammation; insufficient muscle regeneration and dysregulated protein and organelle maintenance. Previous investigative therapeutics tended to isolate and focus on just one of these targets and, consequently, therapeutic activity has been limited. Nuclear erythroid 2-related factor 2 (Nrf2) is a transcription factor that upregulates many cytoprotective gene products in response to oxidants and other toxic stressors. Unlike other strategies, targeted Nrf2 activation has the potential to simultaneously modulate separate pathological features of DMD to amplify therapeutic benefits. Here, we review the literature providing theoretical context for targeting Nrf2 as a disease modifying treatment against DMD.
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