Duchenne muscular dystrophy (DMD) is a lethal X-linked musculodegenerative condition
consisting of an underlying genetic defect whose manifestation is augmented by
inflammatory mechanisms. Previous treatment approaches using gene replacement, exon-
skipping or allogeneic cell therapy have been relatively unsuccessful. The only intervention
to mediate improvement in survival, albeit minor, is glucocorticoid treatment. Given this
modality appears to function via suppression of underlying inflammation; we focus this …