Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy

Kourakis, Stephanie ORCID: 0000-0001-5683-9989, Timpani, Cara ORCID: 0000-0003-4567-4319, de Haan, Judy B, Gueven, Nuri, Fischer, Dirk and Rybalka, Emma ORCID: 0000-0002-4854-0036 (2021) Targeting Nrf2 for the treatment of Duchenne Muscular Dystrophy. Redox Biology, 38. ISSN 2213-2317

Abstract

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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Item type Article
URI https://vuir.vu.edu.au/id/eprint/42098
DOI https://doi.org/10.1016/j.redox.2020.101803
Official URL https://sciencedirect.com/science/article/pii/S221...
Subjects Historical > FOR Classification > 1109 Neurosciences
Current > Division/Research > Institute for Health and Sport
Current > Division/Research > College of Health and Biomedicine
Keywords redox homeostasis; oxidative stress ; reactive oxygen species ; Duchenne Muscular Dystrophy ; DMD ; neuromuscular disease ; neurodegenerative disease ; metabolic diseases
Citations in Scopus 10 - View on Scopus
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