Neuronal nitric oxide synthase (nNOS) splice variant function: Insights into nitric oxide signaling from skeletal muscle

摘要: Defects in neuronal nitric oxide synthase (nNOS) splice variant localization and signaling skeletal muscle are a firmly established pathogenic characteristic of many neuromuscular diseases, including Duchenne Becker muscular dystrophy (DMD BMD, respectively). Therefore, substantial efforts have been made to understand therapeutically target nNOS isoform signaling. The purpose this review is summarize recent salient advances understanding the regulation, targeting, function nNOSμ nNOSβ variants normal dystrophic muscle, primarily using findings from mouse models. first focus how differential targeting creates spatially functionally distinct (NO) compartments at sarcolemma, Golgi complex, cytoplasm. Particular attention given functions sarcolemmal limitations current knockout second major cGMP-mediated its emergence as therapeutic DMD BMD. Accordingly, we address preclinical clinical successes setbacks with testing phosphodiesterase 5 inhibitors redress defects In summary, aims advance messenger NO harnessed for cellular perspective.