Abstract
Duchenne muscular dystrophy (DMD) is an incurable X-linked disease characterised by progressive muscle weakness and wasting leading to premature death. This thesis explored the role of oxidative stress in the pathophysiology of DMD, with a focus on dystrophic muscle protein thiol oxidation. Experiments were undertaken using the dystrophic mdx mouse and GRMD dog models, and a novel dystrophic mouse strain with enhanced exercise capability. The results of this thesis suggest that reducing dystrophic muscle protein thiol oxidation could reduce the functional deficits seen in dystrophic muscle and reduce the severity and progression of the disease.
Original language | English |
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Qualification | Doctor of Philosophy |
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Award date | 15 Oct 2019 |
DOIs | |
Publication status | Unpublished - 2019 |
Embargo information
- Embargoed from 17/10/2019 to 31/05/2021. Made publicly available on 31/05/2021.