Mechanisms stimulating protein degradation to cause muscle atrophy.
Catabolic conditions such as uremia, cancer, insulin-dependent diabetes and sepsis are associated with muscle atrophy resulting from activation of the ubiquitin-proteasome proteolytic pathway. Evidence for the activation of this pathway includes an increase in both proteolytic activity and capacity, as demonstrated by increased protein degradation and a higher rate of gene transcription in muscle yielding increased levels of mRNAs encoding components of the pathway. Glucocorticoids are critical but other hormones and cytokines interact to regulate the activity of this proteolytic pathway.
Price
S R
SR
Renal Division, Emory University, Atlanta, GA 30322, USA.
Mitch
W E
WE
D000818:Animals; D003546:Cysteine Endopeptidases / Q000378:metabolism; D006801:Humans; D009097:Multienzyme Complexes / Q000378:metabolism; D009133:Muscular Atrophy / Q000209:etiology* / Q000378:metabolism*; D046988:Proteasome Endopeptidase Complex; D011506:Proteins / Q000235:genetics / Q000378:metabolism*; D014158:Transcription, Genetic; D014452:Ubiquitins / Q000378:metabolism
D009097:Multienzyme Complexes; D011506:Proteins; D014452:Ubiquitins; D003546:Cysteine Endopeptidases; D046988:Proteasome Endopeptidase Complex