Mechanisms of apoptosis in the heart

被引：140

作者：

Gustafsson, ÅB ^{[1
]}

Gottlieb, RA ^{[1
]}

机构：

[1] Scripps Res Inst, Dept Mol & Expt Med, MEM 220, La Jolla, CA 92037 USA

来源：

JOURNAL OF CLINICAL IMMUNOLOGY | 2003年 / 23卷 / 06期

关键词：

apoptosis; cardiac myocytes; mitochondria; death receptors; ACTIVATED PROTEIN-KINASE; NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; FAS-MEDIATED APOPTOSIS; MITOCHONDRIAL PERMEABILITY TRANSITION; SIGNAL-TRANSDUCTION PATHWAYS; CASPASE RECRUITMENT DOMAIN; CULTURED CARDIAC MYOCYTES; HYPOXIA INDUCES APOPTOSIS; RAT VENTRICULAR MYOCYTES;

D O I：

10.1023/B:JOCI.0000010421.56035.60

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Apoptosis is a complex and highly regulated form of cell death, and believed to contribute to the continuous decline of ventricular function in heart failure. Apoptotic cell death is observed in a variety of cardiovascular diseases, including myocardial infarction, ischemia-reperfusion injury, end-stage heart failure, arrhythmias, and adriamycin cardiomyopathy. There are several pathways leading to programmed cell death. Apoptosis can be initiated by extracellular or intracellular stimuli, leading to the activation of caspases and subsequent cell death. A better understanding of the process of apoptosis in the heart is clearly important as it may lead to the identification of novel therapies for cardiovascular disease. This review is focused on the basic cellular mechanisms of apoptosis, as well as our current understanding of this process in the heart.

引用

页码：447 / 459

页数：13

共 172 条

[1] The Bcl-2 protein family: Arbiters of cell survival [J].

Adams, JM ;

Cory, S .

SCIENCE, 1998, 281 (5381) :1322-1326

[2] Enhanced Gαq signaling:: A common pathway mediates cardiac hypertrophy and apoptotic heart failure [J].

Adams, JW ;

Sakata, Y ;

Davis, MG ;

Sah, VP ;

Wang, YB ;

Liggett, SB ;

Chien, KR ;

Brown, JH ;

Dorn, GW .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (17) :10140-10145

[3] Oxidative stress activates extracellular signal-regulated kinases through Src and ras in cultured cardiac myocytes of neonatal rats [J].

Aikawa, R ;

Komuro, I ;

Yamazaki, T ;

Zou, YZ ;

Kudoh, S ;

Tanaka, M ;

Shiojima, I ;

Hiroi, Y ;

Yazaki, Y .

JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (07) :1813-1821

[4] Direct activation of mitochondrial apoptosis machinery by c-Jun N-terminal kinase in adult cardiac myocytes [J].

Aoki, H ;

Kang, PM ;

Hampe, J ;

Yoshimura, K ;

Noma, T ;

Matsuzaki, M ;

Izumo, S .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (12) :10244-10250

[5] ULTRASTRUCTURAL QUANTITATION OF MITOCHONDRIA AND MYOFILAMENTS IN CARDIAC-MUSCLE FROM 10 DIFFERENT ANIMAL SPECIES INCLUDING MAN [J].

BARTH, E ;

STAMMLER, G ;

SPEISER, B ;

SCHAPER, J .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1992, 24 (07) :669-681

[6] An essential role for NF-kappa B in preventing TNF-alpha-induced cell death [J].

Beg, AA ;

Baltimore, D .

SCIENCE, 1996, 274 (5288) :782-784

[7] The mitochondrial apoptotic pathway is activated by serum and glucose deprivation in cardiac myocytes [J].

Bialik, S ;

Cryns, VL ;

Drincic, A ;

Miyata, S ;

Wollowick, AL ;

Srinivasan, A ;

Kitsis, RN .

CIRCULATION RESEARCH, 1999, 85 (05) :403-414

[8] Stimulation of the stress-activated mitogen-activated protein kinase subfamilies in perfused heart - p38/RK mitogen-activated protein kinases and c-Jun N-terminal kinases are activated by ischemia/reperfusion [J].

Bogoyevitch, MA ;

GillespieBrown, J ;

Ketterman, AJ ;

Fuller, SJ ;

BenLevy, R ;

Ashworth, A ;

Marshall, CJ ;

Sugden, PH .

CIRCULATION RESEARCH, 1996, 79 (02) :162-173

[9] Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death [J].

Boldin, MP ;

Goncharov, TM ;

Goltsev, YV ;

Wallach, D .

CELL, 1996, 85 (06) :803-815

[10] Release of cytochrome c from heart mitochondria is induced by high Ca2+ and peroxynitrite and is responsible for Ca2+-induced inhibition of substrate oxidation [J].

Borutaite, V ;

Morkuniene, R ;

Brown, GC .

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1999, 1453 (01) :41-48

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