The LINC complex, that couples the interphase cytoskeleton to the nucleus, regulates the processing of a cluster of miRNAs required for muscle regeneration by recruiting and interacting directly with Drosha.
Genetic and biochemical analyses reveal that PERK is important for the survival of activated satellite stem cells during regeneration of injured skeletal muscle.
The concepts that oxidative muscle fibres cannot be large and that satellite cell number is the major determinant for effective regeneration are fundamentally challenged.
Modulation of muscle stem cell redox state in culture both improves their amplification while maintaining a similar grafting potential as freshly isolated stem cells.
Inhibition of Polo-like kinase that has been shown to exhibit antitumor effect unexpectedly disrupts muscle stem cell function, leading to developmental and regenerative failures.
Ablation of canonical TGFβ signaling in muscle stem cells at any age is detrimental, and not beneficial, to effective skeletal muscle regeneration due to the promotion of premature fate commitment at the expense of progenitor amplification.
Skeletal muscle stem cells play important roles in the regeneration of neuromuscular junctions, and so present new targets for therapies to treat neuromuscular decline observed in the context of aging and various neuromuscular diseases.
A set of ex vivo and in vivo experiments, including genetic ablation and regeneration studies, identify a key regulatory function of SOXF factors in muscle stem cells in mice.
The regulatory programs governing skeletal muscle regeneration that are controlled by Klf5 in cooperation with MyoD and Mef2 provide a potential avenue for intervention into muscle regeneration through modulation of Klf5.
Building on previous work (Liu et al., 2015), it is shown that depletion or rescue of adult skeletal muscle stem cells is sufficient to induce or attenuate age-associated neuromuscular junction deterioration respectively.
