Erratum: Immortalized human myotonic dystrophy type 1 muscle cell lines to address patient heterogeneity.

[This corrects the article DOI: 10.1016/j.isci.

Peroxiredoxin 2 mediates redox-stimulated adaptations to oxidative phosphorylation induced by contractile activity in human skeletal muscle myotubes.

Skeletal muscle generates superoxide during contractions, which is converted to hydrogen peroxide (HO). HO has been proposed to activate signalling pathways and transcription factors that regulate adaptive responses to exercise, but the concentration required to oxidize and activate key redox-sensitive signalling proteins in vitro is much higher than the typical intracellular levels seen in muscle after exercise. We hypothesized that 2-Cys-peroxiredoxins (PRDX), which rapidly oxidize in the presence of physiological concentrations of HO, serve as intermediary signalling molecules and play a crucial role in activating adaptive pathways following muscle contractions.

Author Correction: Cell-mediated exon skipping normalizes dystrophin expression and muscle function in a new mouse model of Duchenne Muscular Dystrophy.

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Different outcomes of endurance and resistance exercise in skeletal muscles of Oculopharyngeal muscular dystrophy.

Background: Exercise is widely considered to have beneficial impact on skeletal muscle aging. In addition, there are also several studies demonstrating a positive effect of exercise on muscular dystrophies. Oculopharyngeal muscular dystrophy (OPMD) is a late-onset autosomal dominant inherited neuromuscular disorder caused by mutations in the PAPBN1 gene.