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Fig. 1 | Orphanet Journal of Rare Diseases

Fig. 1

From: Therapeutic strategies to address neuronal nitric oxide synthase deficiency and the loss of nitric oxide bioavailability in Duchenne Muscular Dystrophy

Fig. 1

Schematic of methods utilised to increase NO bioavailability in dystrophic skeletal muscle and the downstream effects. Increasing NO bioavailability through (1) restoration of nNOS, (2) ˪-arginine supplementation, (3) NO donation and (4) inhibition of the enzyme phosphodiesterase (PDE) has led to increases in mitochondrial function, exercise capacity and stabilisation of the membrane in dystrophin-deficient skeletal muscle. A potential consequence of increased NO bioavailability, as observed through nitrate supplementation (5), is peroxynitrite (ONOO) formation which can lead to further muscle damage and is undesirable in dystrophic skeletal muscle

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