title: Muscle atrophy in chronic kidney disease results from abnormalities in insulin signaling.
abstract: Muscle atrophy is a significant consequence of chronic kidney disease that increases a patient's risk of mortality and decreases their quality of life. The loss of lean body mass results, in part, from an increase in the rate of muscle protein degradation. In this review, the proteolytic systems that are activated during chronic kidney disease and the key insulin signaling pathways that regulate the protein degradative processes are described.
authors.affiliation: Renal Division, School of Medicine, Emory University, Atlanta, Georgia 30322, USA. russ.price@emory.edu
authors.forename: S Russ
authors.initials: SR
authors.lastname: Price
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Gooch
authors.forename: Sue K
authors.initials: SK
authors.lastname: Donaldson
authors.forename: Tiffany K
authors.initials: TK
authors.lastname: Roberts-Wilson
mesh_terms: D000138:Acidosis / Q000150:complications; D000818:Animals; D002908:Chronic Disease; D005938:Glucocorticoids / Q000096:biosynthesis; D006801:Humans; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007674:Kidney Diseases / Q000150:complications*; D009124:Muscle Proteins / Q000378:metabolism; D009133:Muscular Atrophy / Q000209:etiology*; D010447:Peptide Hydrolases / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D005938:Glucocorticoids; D007328:Insulin; D009124:Muscle Proteins; D007334:Insulin-Like Growth Factor I; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D010447:Peptide Hydrolases
references.citation: Am J Physiol Renal Physiol. 2004 Oct;287(4):F700-6
references.pmid: 15161606
references.citation: J Biol Chem. 1997 Mar 14;272(11):7455-63
references.pmid: 9054447
references.citation: Am J Physiol. 1994 Oct;267(4 Pt 1):C955-60
references.pmid: 7943291
references.citation: Mol Cell. 2004 May 7;14(3):395-403
references.pmid: 15125842
references.citation: J Clin Invest. 2009 Oct;119(10):3059-69
references.pmid: 19759515
references.citation: Cell Metab. 2007 Dec;6(6):472-83
references.pmid: 18054316
references.citation: J Biol Chem. 2002 May 10;277(19):16673-81
references.pmid: 11872750
references.citation: Cell. 2004 Apr 30;117(3):399-412
references.pmid: 15109499
references.citation: Kidney Int. 2007 Jan;71(2):146-52
references.pmid: 17063174
references.citation: J Clin Invest. 2004 Jan;113(1):115-23
references.pmid: 14702115
references.citation: J Am Soc Nephrol. 2006 Nov;17(11):3233-9
references.pmid: 17005936
references.citation: J Clin Invest. 1996 Feb 15;97(4):1064-75
references.pmid: 8613530
references.citation: Am J Physiol. 1995 Sep;269(3 Pt 1):C706-12
references.pmid: 7573401
references.citation: J Am Soc Nephrol. 2006 May;17(5):1388-94
references.pmid: 16611720
references.citation: Am J Physiol. 1987 May;252(5 Pt 1):E621-6
references.pmid: 3578511
references.citation: Proc Natl Acad Sci U S A. 1996 Mar 5;93(5):1967-71
references.pmid: 8700868
references.citation: Am J Physiol Renal Physiol. 2007 Feb;292(2):F660-6
references.pmid: 16954342
references.citation: Exp Nephrol. 2002;10(4):285-92
references.pmid: 12097832
references.citation: FASEB J. 2004 Jan;18(1):39-51
references.pmid: 14718385
references.citation: J Clin Invest. 1987 Apr;79(4):1099-103
references.pmid: 3549778
references.citation: Am J Kidney Dis. 2001 Dec;38(6):1337-42
references.pmid: 11728972
references.citation: J Clin Invest. 1986 Feb;77(2):614-21
references.pmid: 3511100