Linked Life Data

14657508

Source:http://linkedlifedata.com/resource/pubmed/id/14657508

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
48
pubmed:dateCreated
2003-12-5
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1539-6150
pubmed:author
pubmed:issnType
Electronic
pubmed:day
3
pubmed:volume
2003
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
pe34
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Does the road to muscle rejuvenation go through Notch?
pubmed:affiliation
Boston Biomedical Research Institute, 64 Grove Street, Watertown, MA 02472, USA.
pubmed:publicationType
Journal Article, Review