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.
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.
Mice deficient in the TRPM6 channel suffer from impaired prenatal development, shortened lifespan, growth deficit and disturbed energy balance due to a defect in epithelial Mg2+ uptake, thus highlighting a pivotal role of TRPM6 in organismal Mg2+ homeostasis.
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.