Cardiomyocyte apoptosis in hypertensive cardiomyopathy

被引:102
作者
González, A
Fortuño, MA
Querejeta, R
Ravassa, S
López, B
López, N
Díez, J
机构
[1] Univ Navarra, Fac Med, Div Fisiopatol Cardiovasc, Sch Med,Ctr Appl Med Res, E-31080 Pamplona, Spain
[2] Donostia Univ Hosp, San Sebastian, Spain
[3] Univ Navarra Clin, Sch Med, Dept Cardiol & Cardiovasc Surg, Pamplona, Spain
关键词
apoptosis; arterial hypertension; cardiomyocytes; heart failure;
D O I
10.1016/S0008-6363(03)00498-X
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It is widely accepted that there are two principal forms of cell death; namely, necrosis and apoptosis. According to the classical view, necrosis is the major mechanism of cardiomyocyte death in cardiac diseases. However, in the past few years observations have been made showing that cardiomyocyte apoptosis occurs in diverse conditions and that apoptosis may be a contributing cause of the loss and functional abnormalities of cardiomyocytes with important pathophysiological consequences. In this regard, although a number of formal proofs are pending, it is conceivable that cardiomyocyte apoptosis may be an important variable in the clinical evolution of hypertensive cardiomyopathy. This review summarizes recent evidence demonstrating that cardiomyocyte apoptosis is abnormally stimulated in the heart of animals and humans with arterial hypertension. In addition, the potential mechanisms of cardiomyocyte apoptosis in hypertension and its detrimental impact on cardiac function will be addressed. Finally, the perspectives of strategies aimed to detect and modulate apoptosis of cardiomyocytes in hypertensive cardiomyopathy will be considered. (C) 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:549 / 562
页数:14
相关论文
共 181 条
[81]   The calpain family and human disease [J].
Huang, YH ;
Wang, KKW .
TRENDS IN MOLECULAR MEDICINE, 2001, 7 (08) :355-362
[82]   Mechanisms of disease - Signaling pathways for cardiac hypertrophy and failure [J].
Hunter, JJ ;
Chien, KR .
NEW ENGLAND JOURNAL OF MEDICINE, 1999, 341 (17) :1276-1283
[83]   Relationship between cardiomyocyte cell death and cardiac function during hypertensive cardiac remodelling in Dahl rats [J].
Ikeda, S ;
Hamada, M ;
Qu, P ;
Hiasa, G ;
Hashida, H ;
Shigematsu, Y ;
Hiwada, K .
CLINICAL SCIENCE, 2002, 102 (03) :329-335
[84]   Cellular FLIP is expressed in cardiomyocytes and down-regulated in TUNEL-positive grafted cardiac tissues [J].
Imanishi, T ;
Murry, CE ;
Reinecke, H ;
Hano, T ;
Nishio, I ;
Liles, WC ;
Hofsta, L ;
Kim, K ;
O'Brien, KD ;
Schwartz, SM ;
Han, DKM .
CARDIOVASCULAR RESEARCH, 2000, 48 (01) :101-110
[85]  
Ing DJ, 1999, CIRC RES, V84, P21
[86]   Apoptosis as a possible cause of wall thinning in end-stage hypertrophic cardiomyopathy [J].
Ino, T ;
Nishimoto, K ;
Okubo, M ;
Akimoto, K ;
Yabuta, K ;
Kawai, S ;
Okada, R ;
Sueyoshi, N .
AMERICAN JOURNAL OF CARDIOLOGY, 1997, 79 (08) :1137-&
[87]   Apoptosis in cardiac disease [J].
James, TN .
AMERICAN JOURNAL OF MEDICINE, 1999, 107 (06) :606-620
[88]   Apoptosis as a possible cause of gradual development of complete heart block and fatal arrhythmias associated with absence of the AV node, sinus node, and internodal pathways [J].
James, TN ;
Martin, ES ;
Willis, PW ;
Lohr, TO .
CIRCULATION, 1996, 93 (07) :1424-1438
[89]   NORMAL AND ABNORMAL CONSEQUENCES OF APOPTOSIS IN THE HUMAN HEART - FROM POSTNATAL MORPHOGENESIS TO PAROXYSMAL ARRHYTHMIAS [J].
JAMES, TN .
CIRCULATION, 1994, 90 (01) :556-573
[90]  
Jeremias I, 2000, CIRCULATION, V102, P915