Abstract
microRNAs (miRNAs) are small non-coding RNAs required for the post-transcriptional control of gene expression. MicroRNAs play a critical role in modulating muscle regeneration and stem cell behavior. Muscle regeneration is affected in muscular dystrophies, and a critical point for the development of effective strategies for treating muscle disorders is optimizing approaches to target muscle stem cells in order to increase the ability to regenerate lost tissue. Within this framework, miRNAs are emerging as implicated in muscle stem cell response in neuromuscular disorders and new methodologies to regulate the expression of key microRNAs are coming up. In this review, we summarize recent advances highlighting the potential of miRNAs to be used in conjunction with gene replacement therapies, in order to improve muscle regeneration in the context of Duchenne Muscular Dystrophy (DMD).
Highlights
One-half of the body’s mass is composed of skeletal muscles that have important functions basic to life, such as locomotion, postural behavior and breathing
In vitro analysis by using C2C12 myoblast cell line demonstrated that myoblasts proliferation is induced partially by miR-195 and miR-497 repression mediated by proliferative inductors such as NF-κB [58,59,60], leading to an increase of miR-195-miR-497 targets: the cell cycle genes Cyclin E1 (Ccne1), and Cyclin D2 (Ccnd2), and the mitogens Insulin-like growth factor I receptor (Igf1r) and Insulin receptor (Insr) [61]
Duchenne Muscular Dystrophy (DMD) is a disease caused by a mutation in a gene named dystrophin that gets worse over time, with a severe prognosis, and for which there is currently no cure
Summary
One-half of the body’s mass is composed of skeletal muscles that have important functions basic to life, such as locomotion, postural behavior and breathing. The adult mammalian skeletal muscle is one of the few tissues capable of efficient regeneration in response to injury or damage This ability is due, at least partly, to a population of undifferentiated mononuclear myogenic progenitor cells, known as satellite stem cells [1], which reside between the basal lamina and sarcolemma of myofibers. Satellite cells (SCs) are mitotically quiescent, they activate in response to injury or increased contractile activity, thereby re-entering into the cell cycle, proliferating, differentiating, fusing and, regenerating myofibers [2,3] Genetic dissection of this process has revealed that developmental pathways required for embryonic myogenesis regulate muscle regeneration [4,5].
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