Nitric oxide (NO) and duchenne muscular dystrophy: NO way to go?

Timpani, Cara ORCID: 0000-0003-4567-4319, Mamchaoui, K, Butler-Browne, G and Rybalka, Emma ORCID: 0000-0002-4854-0036 (2020) Nitric oxide (NO) and duchenne muscular dystrophy: NO way to go? Antioxidants, 9 (12). pp. 1-8. ISSN 2076-3921

Abstract

The discordance between pre-clinical success and clinical failure of treatment options for Duchenne Muscular Dystrophy (DMD) is significant. The termination of clinical trials investigating the phosphodiesterase inhibitors, sildenafil and tadalafil (which prolong the second messenger molecule of nitric oxide (NO) signaling), are prime examples of this. Both attenuated key dystrophic features in the mdx mouse model of DMD yet failed to modulate primary outcomes in clinical settings. We have previously attempted to modulate NO signaling via chronic nitrate supplementation of the mdx mouse but failed to demonstrate beneficial modulation of key dystrophic features (i.e., metabolism). Instead, we observed increased muscle damage and nitrosative stress which exacerbated MD. Here, we highlight that acute nitrite treatment of human DMD myoblasts is also detrimental and suggest strategies for moving forward with NO replacement therapy in DMD.

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Item type Article
URI https://vuir.vu.edu.au/id/eprint/42096
DOI https://doi.org/10.3390/antiox9121268
Official URL https://www.mdpi.com/2076-3921/9/12/1268
Subjects Historical > FOR Classification > 0601 Biochemistry and Cell Biology
Historical > FOR Classification > 1109 Neurosciences
Current > Division/Research > Institute for Health and Sport
Keywords mitochondrial viability, functional indices, superoxide production, extracellular acidification rate
Citations in Scopus 3 - View on Scopus
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