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Lookup NU author(s): Professor Giorgio TascaORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).In recent years, growing evidence has suggested a prominent role of oxidative stress in the pathophysiology of several early-and adult-onset muscle disorders, although effective antioxidant treatments are still lacking. Oxidative stress causes cell damage by affecting protein function, membrane structure, lipid metabolism, and DNA integrity, thus interfering with skeletal muscle homeostasis and functionality. Some features related to oxidative stress, such as chronic inflammation, defective regeneration, and mitochondrial damage are shared among most muscular dystrophies, and Nrf2 has been shown to be a central player in antagonizing redox imbalance in several of these disorders. However, the exact mechanisms leading to overproduction of reactive oxygen species and deregulation in the cellular antioxidants system seem to be, to a large extent, disease-specific, and the clarification of these mechanisms in vivo in humans is the cornerstone for the development of targeted antioxidant therapies, which will require testing in appropriately designed clinical trials.
Author(s): Mosca N, Petrillo S, Bortolani S, Monforte M, Ricci E, Piemonte F, Tasca G
Publication type: Review
Publication status: Published
Journal: Cells
Year: 2021
Volume: 10
Issue: 6
Online publication date: 01/06/2021
Acceptance date: 28/05/2021
ISSN (electronic): 2073-4409
Publisher: MDPI
URL: https://doi.org/10.3390/cells10061364
DOI: 10.3390/cells10061364
PubMed id: 34205993
