title: Muscle protein kinetics in cancer cachexia.
abstract: OBJECTIVE
  Skeletal muscle loss appears to be the most significant event in cancer cachexia and is associated with a poor outcome. The balance between mechanisms that control synthesis and degradation is fundamental when designing new therapies. This review aims to highlight the molecular mechanisms that are associated with protein kinetics.
  
  
  RESULTS
  The mechanisms that promote muscle synthesis have been explored in detail recently but moreover they have been the mechanisms behind degradation. Specific advances in cellular signalling molecules related to autophagy pathways including signal transducer and activators of transcription-3, activin type-2 receptor, TRAF6, and transcriptomic research have been given special attention in this review to highlight their roles in degradation and as potential targets for therapeutics. Ways to quantify muscle loss are badly needed for outcome measures; recent research using radiolabelled amino acids has also been discussed in this review.
  
  
  CONCLUSIONS
  Only by having an appreciation of the complex regulation of muscle protein synthesis and degradation, will potential new therapeutics be able to be developed. This review identifies known targets in molecular pathways of current interest, explores methods used to find novel genes which may be involved in muscle kinetics and also highlights ways in which muscle kinetics may be measured to assess the efficacy of such interventions.
authors.affiliation: Department of Clinical Surgery, University of Edinburgh, Edinburgh, Scotland, UK.
authors.forename: Neil
authors.initials: N
authors.lastname: Johns
authors.forename: Nathan A
authors.initials: NA
authors.lastname: Stephens
authors.forename: Tom
authors.initials: T
authors.lastname: Preston
mesh_terms: D030301:Activin Receptors, Type II / Q000378:metabolism; D000328:Adult; D002100:Cachexia / Q000209:etiology / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D009124:Muscle Proteins / Q000096:biosynthesis* / Q000235:genetics; D009133:Muscular Atrophy / Q000209:etiology / Q000235:genetics / Q000378:metabolism*; D009369:Neoplasms / Q000150:complications*; D059748:Proteolysis; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics; D048029:TNF Receptor-Associated Factor 6 / Q000378:metabolism
chemical_list: D009124:Muscle Proteins; D050796:STAT3 Transcription Factor; D048029:TNF Receptor-Associated Factor 6; D030301:Activin Receptors, Type II