The involvement of the ubiquitin proteasome system in human skeletal muscle remodelling and atrophy

被引：203

作者：

Murton, A. J. ^{[1
]}

Constantin, D. ^{[1
]}

Greenhaff, P. L. ^{[1
]}

机构：

[1] Univ Nottingham, Queens Med Ctr, Sch Biomed Sci, Ctr Integrated Syst Biol & Med, Nottingham NG7 2RD, England

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2008年 / 1782卷 / 12期

关键词：

Exercise; Skeletal muscle; Atrophy; Inflammation; Ubiquitin proteasome system; Human;

D O I：

10.1016/j.bbadis.2008.10.011

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Skeletal muscle exhibits great plasticity in response to altered activity levels, ultimately resulting ill tissue remodelling and substantial changes in mass. Animal research would suggest that the ubiquitin proteasome system. ill particular the ubiquitin ligases MAFbx/atrogin-1 and MuRF1, are instrumental to the processes underlying these changes. This review article therefore examines the role of proteasomal-mediated protein degradation in human skeletal muscle in health and disease. Specifically, the effects of exercise. disuse and inflammatory disease states oil the ubiquitin proteasome system in human skeletal muscle are examined. The article also identifies several inconsistencies between Published human studies and data obtained from animal models of muscle atrophy, highlighting the need for a more comprehensive examination of the molecular events responsible for modulating muscle mass in humans. (C) 2008 Elsevier B.V. All rights reserved.

引用

页码：730 / 743

页数：14

共 170 条

[1] Eccentric exercise decreases maximal insulin action in humans: Muscle and systemic effects [J].

Asp, S ;

Daugaard, JR ;

Kristiansen, S ;

Kiens, B ;

Richter, EA .

JOURNAL OF PHYSIOLOGY-LONDON, 1996, 494 (03) :891-898

[2] The ubiquitin-proteasome system and skeletal muscle wasting [J].

Attaix, D ;

Ventadour, S ;

Codran, A ;

Béchet, D ;

Taillandier, D ;

Combaret, L .

ESSAYS IN BIOCHEMISTRY, VOL 41: THE UBIQUITIN-PROTEASOME SYSTEM, 2005, 41 :173-186

[3]

Attaix Didier, 2003, P219, DOI 10.1079/9780851996790.0219

[4] The acidosis of chronic renal failure activates muscle proteolysis in rats by augmenting transcription of genes encoding proteins of the ATP-dependent ubiquitin-proteasome pathway [J].

Bailey, JL ;

Wang, XN ;

England, BK ;

Price, SR ;

Ding, XY ;

Mitch, WE .

JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (06) :1447-1453

[5]

Bamman MM, 2001, AM J PHYSIOL-ENDOC M, V280, pE383

[6] Cytokine profile in quadriceps muscles of patients with severe COPD [J].

Barreiro, E. ;

Schols, A. M. W. J. ;

Polkey, M. I. ;

Galdiz, J. B. ;

Gosker, H. R. ;

Swallow, E. B. ;

Coronell, C. ;

Gea, J. .

THORAX, 2008, 63 (02) :100-107

[7] Calpains in muscle wasting [J].

Bartoli, M ;

Richard, I .

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2005, 37 (10) :2115-2133

[8] Lysosomal proteolysis in skeletal muscle [J].

Bechet, D ;

Tassa, A ;

Taillandier, D ;

Cornbaret, L ;

Attaix, D .

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2005, 37 (10) :2098-2114

[9] EUGLYCEMIC HYPERINSULINEMIA AUGMENTS AMINO-ACID-UPTAKE BY HUMAN LEG TISSUES DURING HYPERAMINOACIDEMIA [J].

BENNET, WM ;

CONNACHER, AA ;

SCRIMGEOUR, CM ;

JUNG, RT ;

RENNIE, MJ .

AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (02) :E185-E194

[10] Oxandrolone in AIDS-wasting myopathy [J].

Berger, JR ;

Pall, L ;

Hall, CD ;

Simpson, DM ;

Berry, PS ;

Dudley, R .

AIDS, 1996, 10 (14) :1657-1662

← 1 2 3 4 5 6 7 8 9 10 →