Hypertrophy and atrophy of the heart - The other side of remodeling

被引:25
作者
Razeghi, Peter [1 ]
Taegtmeyer, Heinrich [1 ]
机构
[1] Univ Texas, Sch Med, Div Cardiol, Houston, TX 77030 USA
来源
INTERACTIVE AND INTEGRATIVE CARDIOLOGY | 2006年 / 1080卷
关键词
atrophy; ubiquitin; proteasome; remodeling;
D O I
10.1196/annals.1380.011
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The size of a cardiomyocyte is determined by relative rates of protein synthesis and degradation. Signaling pathways regulating myocardial protein synthesis have been extensively investigated, not the least because in patients hypertrophy increases cardiovascular morbidity and mortality. Until now strategies to reverse hypertrophy have relied on the inhibition of prohypertrophic signaling pathways. Here we review signaling pathways of atrophy in the heart and we present evidence in support of the idea that activating proatrophic signaling pathways in the presence of prohypertrophic signaling may be an attractive strategy to reverse hypertrophy.
引用
收藏
页码:110 / 119
页数:10
相关论文
共 53 条
[1]   Muscle ring finger protein-1 inhibits PKCε activation and prevents cardiomyocyte hypertrophy [J].
Arya, R ;
Kedar, V ;
Hwang, JR ;
McDonough, H ;
Li, HH ;
Taylor, J ;
Patterson, C .
JOURNAL OF CELL BIOLOGY, 2004, 167 (06) :1147-1159
[2]   Identification of ubiquitin ligases required for skeletal muscle atrophy [J].
Bodine, SC ;
Latres, E ;
Baumhueter, S ;
Lai, VKM ;
Nunez, L ;
Clarke, BA ;
Poueymirou, WT ;
Panaro, FJ ;
Na, EQ ;
Dharmarajan, K ;
Pan, ZQ ;
Valenzuela, DM ;
DeChiara, TM ;
Stitt, TN ;
Yancopoulos, GD ;
Glass, DJ .
SCIENCE, 2001, 294 (5547) :1704-1708
[3]   HEAT-STABLE POLYPEPTIDE COMPONENT OF AN ATP-DEPENDENT PROTEOLYTIC SYSTEM FROM RETICULOCYTES [J].
CIECHANOVER, A ;
HOD, Y ;
HERSHKO, A .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1978, 81 (04) :1100-1105
[4]   Unloaded heart in vivo replicates fetal gene expression of cardiac hypertrophy [J].
Depre, C ;
Shipley, GL ;
Chen, WH ;
Han, QY ;
Doenst, T ;
Moore, ML ;
Stepkowski, S ;
Davies, PJA ;
Taegtmeyer, H .
NATURE MEDICINE, 1998, 4 (11) :1269-1275
[5]   Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress [J].
Esposito, G ;
Rapacciuolo, A ;
Prasad, SVN ;
Takaoka, H ;
Thomas, SA ;
Koch, WJ ;
Rockman, HA .
CIRCULATION, 2002, 105 (01) :85-92
[6]   Hypertrophy of the heart - A new therapeutic target? [J].
Frey, N ;
Katus, HA ;
Olson, EN ;
Hill, JA .
CIRCULATION, 2004, 109 (13) :1580-1589
[7]   Nobel committee tags ubiquitin for distinction [J].
Goldberg, AL .
NEURON, 2005, 45 (03) :339-344
[8]   EFFECTS OF AGING AND LONG-TERM DIETARY INTERVENTION ON PROTEIN-TURNOVER AND GROWTH OF VENTRICULAR MUSCLE IN THE RAT-HEART [J].
GOLDSPINK, DF ;
LEWIS, SEM ;
MERRY, BJ .
CARDIOVASCULAR RESEARCH, 1986, 20 (09) :672-678
[9]   The calpain system [J].
Goll, DE ;
Thompson, VF ;
Li, HQ ;
Wei, W ;
Cong, JY .
PHYSIOLOGICAL REVIEWS, 2003, 83 (03) :731-801
[10]   Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy [J].
Gomes, MD ;
Lecker, SH ;
Jagoe, RT ;
Navon, A ;
Goldberg, AL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (25) :14440-14445