| Literature DB >> 26385617 |
Erin E Talbert1, Denis C Guttridge2.
Abstract
While changes in muscle protein synthesis and degradation have long been known to contribute to muscle wasting, a body of literature has arisen which suggests that regulation of the satellite cell and its ensuing regenerative program are impaired in atrophied muscle. Lessons learned from cancer cachexia suggest that this regulation is simply not a consequence, but a contributing factor to the wasting process. In addition to satellite cells, evidence from mouse models of cancer cachexia also suggests that non-satellite progenitor cells from the muscle microenvironment are also involved. This chapter in the series reviews the evidence of dysfunctional muscle repair in multiple wasting conditions. Potential mechanisms for this dysfunctional regeneration are discussed, particularly in the context of cancer cachexia.Entities:
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Year: 2015 PMID: 26385617 PMCID: PMC4922677 DOI: 10.1016/j.semcdb.2015.09.009
Source DB: PubMed Journal: Semin Cell Dev Biol ISSN: 1084-9521 Impact factor: 7.727