title: Does the road to muscle rejuvenation go through Notch?
abstract: The capacity of skeletal muscles to repair and regenerate declines during aging in humans, and this decline may lead to muscle loss and frailty. Conboy et al. show that injured muscles of aging mice are defective in Notch signaling, because up-regulation of the Notch ligand, Delta-1, is impaired. Delta-1 promotes proliferation of the satellite cells that repair damaged muscles, and Conboy et al. show that experimental activation of Notch signaling is sufficient to reverse the age-related decline in muscle regenerative capacity. Extension of these important findings to humans could lead to the development of new therapeutic approaches to maintain muscle function during aging.
authors.affiliation: Boston Biomedical Research Institute, 64 Grove Street, Watertown, MA 02472, USA.
authors.forename: Jeffrey Boone
authors.initials: JB
authors.lastname: Miller
authors.forename: Charles P
authors.initials: CP
authors.lastname: Emerson
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D002455:Cell Division / Q000502:physiology; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins / Q000502:physiology*; D018482:Muscle, Skeletal / Q000166:cytology / Q000293:injuries / Q000502:physiology*; D051880:Receptors, Notch; D012038:Regeneration / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D051880:Receptors, Notch; C064045:delta protein