Fig. 1From: Therapeutic strategies to address neuronal nitric oxide synthase deficiency and the loss of nitric oxide bioavailability in Duchenne Muscular DystrophySchematic 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 muscleBack to article page