Abstract

The progressive muscle weakness as observed in Duchenne muscular dystrophy (DMD) is a consequence of dystrophin deficiency. Loss of this functional protein leads to elevated levels of intracellular calcium, a key step in the cellular pathology of DMD. The cysteine protease calpain is activated in dystrophin-deficient muscle, and its inhibition is regarded as a potential therapeutic approach. In addition, previous work has shown that the ubiquitin/proteasome system also contributed to muscle protein breakdown in dystrophic muscle and, therefore, also qualifies as a potential target for therapeutic intervention in DMD.

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