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Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy


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Kourakis, S, Timpani, CA, de Haan, JB, Gueven, N ORCID: 0000-0003-3782-767X, Fischer, D and Rybalka, E 2021 , 'Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy' , Redox Biology , doi: 10.1016/j.redox.2020.101803.

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Imbalances in redox homeostasis can result in oxidative stress, which is implicated in various pathologicalconditions including the fatal neuromuscular disease Duchenne Muscular Dystrophy (DMD). DMD is a complicateddisease, with many druggable targets at the cellular and molecular level including calcium-mediatedmuscle degeneration; mitochondrial dysfunction; oxidative stress; inflammation; insufficient muscle regenerationand dysregulated protein and organelle maintenance. Previous investigative therapeutics tended to isolateand focus on just one of these targets and, consequently, therapeutic activity has been limited. Nuclear erythroid2-related factor 2 (Nrf2) is a transcription factor that upregulates many cytoprotective gene products in responseto oxidants and other toxic stressors. Unlike other strategies, targeted Nrf2 activation has the potential tosimultaneously modulate separate pathological features of DMD to amplify therapeutic benefits. Here, we reviewthe literature providing theoretical context for targeting Nrf2 as a disease modifying treatment against DMD.

Item Type: Article
Authors/Creators:Kourakis, S and Timpani, CA and de Haan, JB and Gueven, N and Fischer, D and Rybalka, E
Keywords: Nrf2, Duchenne Muscular Dystrophy, reactive oxygen species, oxidative stress, skeletal muscle, hormesis
Journal or Publication Title: Redox Biology
Publisher: Elsevier BV
ISSN: 2213-2317
DOI / ID Number: 10.1016/j.redox.2020.101803
Copyright Information:

Copyright 2020 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY license

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