Bcl-2 family members and apoptosis, taken to heart

被引：257

作者：

Gustafsson, Asa B. ^{[1
]}

Gottlieb, Roberta A. ^{[1
]}

机构：

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

来源：

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 2007年 / 292卷 / 01期

关键词：

cardiovascular disease; cytochrome c; protein; mitochondria;

D O I：

10.1152/ajpcell.00229.2006

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Loss of myocardial cells via apoptosis has been observed in many cardiovascular diseases and has been shown to contribute to the initiation and progression of heart failure. The Bcl-2 family members are important regulators of the mitochondrial pathway of apoptosis. These proteins decide whether the mitochondria should initiate the cell death program and release proapoptotic factors such as cytochrome c. The Bcl-2 proteins consist of anti- and proapoptotic members and play a key role in regulating apoptosis in the myocardium. The antiapoptotic proteins have been demonstrated to protect against various cardiac pathologies, whereas the antiapoptotic proteins have been reported to contribute to heart disease. This review summarizes the current understanding of the role of Bcl-2 proteins in the heart.

引用

页码：C45 / C51

页数：7

共 100 条

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

Adams, JM ;

Cory, S .

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

[2] Apoptosis and post-infarction left ventricular remodeling [J].

Baldi, A ;

Abbate, A ;

Bussani, R ;

Patti, G ;

Melfi, R ;

Angelini, A ;

Dobrina, A ;

Rossiello, R ;

Silvestri, F ;

Baldi, F ;

Di Sciascio, G .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2002, 34 (02) :165-174

[3] 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

[4] Bcl-2 and Bax regulate the channel activity of the mitochondrial adenine nucleotide translocator [J].

Brenner, C ;

Cadiou, H ;

Vieira, HLA ;

Zamzami, N ;

Marzo, I ;

Xie, ZH ;

Leber, B ;

Andrews, D ;

Duclohier, H ;

Reed, JC ;

Kroemer, G .

ONCOGENE, 2000, 19 (03) :329-336

[5]

Brocheriou V, 2000, J GENE MED, V2, P326, DOI 10.1002/1521-2254(200009/10)2:5<326::AID-JGM133>3.0.CO

[6]

2-1

[7] Expression of the gene encoding the proapoptotic Nip3 protein is induced by hypoxia [J].

Bruick, RK .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (16) :9082-9087

[8] Bax translocates to mitochondria of heart cells during simulated ischaemia: involvement of AMP-activated and p38 mitogen-activated protein kinases [J].

Capano, M ;

Crompton, M .

BIOCHEMICAL JOURNAL, 2006, 395 :57-64

[9] The first α helix of Bax plays a necessary role in its ligand-induced activation by the BH3-only proteins bid and PUMA [J].

Cartron, PF ;

Gallenne, T ;

Bougras, G ;

Gautier, F ;

Manero, F ;

Vusio, P ;

Meflah, K ;

Vallette, FM ;

Juin, P .

MOLECULAR CELL, 2004, 16 (05) :807-818

[10] Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function [J].

Chen, L ;

Willis, SN ;

Wei, A ;

Smith, BJ ;

Fletcher, JI ;

Hinds, MG ;

Colman, PM ;

Day, CL ;

Adams, JM ;

Huang, DCS .

MOLECULAR CELL, 2005, 17 (03) :393-403

← 1 2 3 4 5 6 7 8 9 10 →