Therapy insight: cardiovascular complications associated with muscular dystrophies

被引:17
作者
McNally, EM [1 ]
MacLeod, H [1 ]
机构
[1] Univ Chicago, Sect Cardiol, Dept Med, Chicago, IL 60637 USA
来源
NATURE CLINICAL PRACTICE CARDIOVASCULAR MEDICINE | 2005年 / 2卷 / 06期
关键词
cardiomyopathy; dystrophin; muscular dystrophy; myotonic dystrophy;
D O I
10.1038/ncpcardio0213
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The muscular dystrophies are commonly associated with cardiovascular complications, including cardiomyopathy and cardiac arrhythmias. These complications are caused by intrinsic defects in cardiomyocyte and cardiac conduction system function, and by the presence of severe skeletal muscle disease, which also contributes to cardiac dysfunction. Unlike the skeletal muscle degenerative process, for which treatment options are currently limited, therapy is available for the cardiovascular complications that accompany muscular dystrophy. New therapies for skeletal muscle degeneration are moving into clinical trials and, ultimately, into clinical practice. These therapies are expected to also improve the cardiac function, longevity and wellbeing of muscular dystrophy patients.
引用
收藏
页码:301 / 308
页数:8
相关论文
共 57 条
[1]   Dysferlin is a plasma membrane protein and is expressed early in human development [J].
Anderson, LVB ;
Davison, K ;
Moss, JA ;
Young, C ;
Cullen, MJ ;
Walsh, J ;
Johnson, MA ;
Bashir, R ;
Britton, S ;
Keers, S ;
Argov, Z ;
Mahjneh, I ;
Fougerousse, F ;
Beckmann, JS ;
Bushby, KMD .
HUMAN MOLECULAR GENETICS, 1999, 8 (05) :855-861
[2]   MLP-deficient mice exhibit a disruption of cardiac cytoarchitectural organization, dilated cardiomyopathy, and heart failure [J].
Arber, S ;
Hunter, JJ ;
Ross, J ;
Hongo, M ;
Sansig, G ;
Borg, J ;
Perriard, JC ;
Chien, KR ;
Caroni, P .
CELL, 1997, 88 (03) :393-403
[3]   Enteroviral protease 2A directly cleaves dystrophin and is inhibited by a dystrophin-based substrate analogue [J].
Badorff, C ;
Berkely, N ;
Mehrotra, S ;
Talhouk, JW ;
Rhoads, RE ;
Knowlton, KU .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (15) :11191-11197
[4]   Defective membrane repair in dysferlin-deficient muscular dystrophy [J].
Bansal, D ;
Miyake, K ;
Vogel, SS ;
Groh, S ;
Chen, CC ;
Williamson, R ;
McNeil, PL ;
Campbell, KP .
NATURE, 2003, 423 (6936) :168-172
[5]   LARGE can functionally bypass α-dystroglycan glycosylation defects in distinct congenital muscular dystrophies [J].
Barresi, R ;
Michele, DE ;
Kanagawa, M ;
Harper, HA ;
Dovico, SA ;
Satz, JS ;
Moore, SA ;
Zhang, WL ;
Schachter, H ;
Dumanski, JP ;
Cohn, RD ;
Nishino, I ;
Campbell, KP .
NATURE MEDICINE, 2004, 10 (07) :696-703
[6]   Muscle-specific expression of insulin-like growth factor I counters muscle decline in mdx mice [J].
Barton, ER ;
Morris, L ;
Musaro, A ;
Rosenthal, N ;
Sweeney, HL .
JOURNAL OF CELL BIOLOGY, 2002, 157 (01) :137-147
[7]   A gene related to Caenorhabditis elegans spermatogenesis factor fer-1 is mutated in limb-girdle muscular dystrophy type 2B [J].
Bashir, R ;
Britton, S ;
Strachan, T ;
Keers, S ;
Vafiadaki, E ;
Lako, M ;
Richard, I ;
Marchand, S ;
Bourg, N ;
Argov, Z ;
Sadeh, M ;
Mahjneh, I ;
Marconi, G ;
Passos-Bueno, MR ;
Moreira, ED ;
Zatz, M ;
Beckmann, JS ;
Bushby, K .
NATURE GENETICS, 1998, 20 (01) :37-42
[8]   Adult cardiac stem cells are multipotent and support myocardial regeneration [J].
Beltrami, AP ;
Barlucchi, L ;
Torella, D ;
Baker, M ;
Limana, F ;
Chimenti, S ;
Kasahara, H ;
Rota, M ;
Musso, E ;
Urbanek, K ;
Leri, A ;
Kajstura, J ;
Nadal-Ginard, B ;
Anversa, P .
CELL, 2003, 114 (06) :763-776
[9]   Intermediate filaments and the function of the dystrophin-protein complex [J].
Blake, DJ ;
Martin-Rendon, E .
TRENDS IN CARDIOVASCULAR MEDICINE, 2002, 12 (05) :224-228
[10]   Functional improvement of dystrophic muscle by myostatin blockade [J].
Bogdanovich, S ;
Krag, TOB ;
Barton, ER ;
Morris, LD ;
Whittemore, LA ;
Ahima, RS ;
Khurana, TS .
NATURE, 2002, 420 (6914) :418-421