Exacerbation of pathology by oxidative stress in respiratory and locomotor muscles with XXXX .

@entity32 @entity82 @entity39 @entity3986 @entity1112 @entity425 @entity2821 @entity1110 @entity1555 @entity13092 @entity4714 @entity15587
@entity1555 ( @entity1555 ) is the most devastating @entity3986 , leading to progressive @entity425 of respiratory (e.g. diaphragm) and locomotor muscles (e.g. gastrocnemius). @entity1555 is caused by @entity1112 in the gene that encodes for @entity4714 , a key scaffolding protein of the dystroglycan complex (DCG) within the sarcolemmal cytoskeleton. As a result of a compromised dystroglycan complex, mechanical integrity is impaired and important signalling proteins (e.g. @entity2821 , @entity15587 ) and pathways are disrupted. Disruption of the dystroglycan complex leads to high susceptibility to injury with repeated, eccentric contractions as well as @entity32 , resulting in significant damage and @entity39 . @entity13092 and repair cycling leads to @entity82 and @entity425 . While the link between @entity32 with damage and @entity425 in the @entity1555 diaphragm is unresolved, elevated oxidative stress may contribute to damage, @entity425 and possibly @entity82 . While utilization of non-specific antioxidant interventions has yielded inconsistent results, recent data suggest that @entity1110 oxidase could play a pivotal role in elevating oxidative stress via integrated changes in @entity15587 and stretch-activated channels (SACs). Oxidative stress may act as an amplifier, exacerbating disruption of the dystroglycan complex, upregulation of the inflammatory transcription factor NF-B, and thus functional impairment of force-generating capacity.
