Apoptosis-related genes expressed in cardiovascular development and disease: an EST approach

被引:18
作者
Rezvani, M
Barrans, JD
Dai, KS
Liew, CC [1 ]
机构
[1] Univ Toronto, Toronto Gen Hosp, Inst Med Sci, Ctr Cardiovasc Res,Univ Hlth Network, Toronto, ON M5G 1L7, Canada
[2] Univ Toronto, Toronto Gen Hosp, Dept Lab Med & Pathobiol, Ctr Cardiovasc Res,Univ Hlth Network, Toronto, ON M5G 1L7, Canada
基金
英国医学研究理事会;
关键词
apoptosis; developmental biology; gene expression; sequence (DNA/RNA/prot);
D O I
10.1016/S0008-6363(99)00383-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Apoptosis (programmmed cell death) is an important process which, in conjunction with cell proliferation, maintains cell number homeostasis, Although apoptosis has been more extensively investigated in other tissues [1,2], only recently has this process been suspected as a significant contributor to both disease and normal development of the cardiovascular system [3-6]. Grasping a comprehension of the underlying genetic mechanisms of apoptosis is especially crucial considering that cardiac myocytes irreversibly exit the cell cycle and thus fail to proliferate during pathological conditions. Despite great strides in understanding the molecular pathways of apoptosis, there still remain numerous questions to be answered. Identifying key genes that are involved in the regulatory process of apoptosis in the cardiovascular system will serve as a basis for creating more effective therapeutic treatments in cardiovascular disease and provide an understanding of how cardiac development is modulated. This review provides a brief summary of recent data implicating genes that may be involved in apoptosis in the cardiovascular system. It also outlines the continued usefulness of large-scale generation of expressed sequence tags (ESTs) to establish expression profiles from the cardiovascular system and as a means of identifying potentially significant apoptotic regulators previously characterized in other tissues but not as yet in the cardiovascular system. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:621 / 629
页数:9
相关论文
共 82 条
[61]   Induction of apoptosis by Apo-2 ligand, a new member of the tumor necrosis factor cytokine family [J].
Pitt, RM ;
Marsters, SA ;
Ruppert, S ;
Donahue, CJ ;
Moore, A ;
Ashkenazi, A .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (22) :12687-12690
[62]   MOLECULAR-CLONING OF A MURINE CDNA-ENCODING A NOVEL PROTEIN, P38-2G4, WHICH VARIES WITH THE CELL-CYCLE [J].
RADOMSKI, N ;
JOST, E .
EXPERIMENTAL CELL RESEARCH, 1995, 220 (02) :434-445
[63]  
REUTELINGSPERGE.C, 1998, MOL BIOL APOPTOSIS I
[64]   The TNFR2-TRAF signaling complex contains two novel proteins related to baculoviral-inhibitor of apoptosis proteins [J].
Rothe, M ;
Pan, MG ;
Henzel, WJ ;
Ayres, TM ;
Goeddel, DV .
CELL, 1995, 83 (07) :1243-1252
[65]   THE GENE FOR NEURONAL APOPTOSIS INHIBITORY PROTEIN IS PARTIALLY DELETED IN INDIVIDUALS WITH SPINAL MUSCULAR-ATROPHY [J].
ROY, N ;
MAHADEVAN, MS ;
MCLEAN, M ;
SHUTLER, G ;
YARAGHI, Z ;
FARAHANI, R ;
BAIRD, S ;
BESNERJOHNSTON, A ;
LEFEBVRE, C ;
KANG, XL ;
SALIH, M ;
AUBRY, H ;
TAMAI, K ;
GUAN, XP ;
IOANNOU, P ;
CRAWFORD, TO ;
DEJONG, PJ ;
SURH, L ;
IKEDA, JE ;
KORNELUK, RG ;
MACKENZIE, A .
CELL, 1995, 80 (01) :167-178
[66]   Mechanisms of cell death in hypoxia/reoxygenation injury [J].
Saikumar, P ;
Dong, Z ;
Weinberg, JM ;
Venkatachalam, MA .
ONCOGENE, 1998, 17 (25) :3341-3349
[67]  
Santoro IM, 1997, CANCER RES, V57, P488
[68]   Isolation of a novel mouse gene MA-3 that is induced upon programmed cell death [J].
Shibahara, K ;
Asano, M ;
Ishida, Y ;
Aoki, T ;
Koike, T ;
Honjo, T .
GENE, 1995, 166 (02) :297-301
[69]   Cardiac genes and gene databases for cardiovascular disease genetics [J].
Tan K.T. ;
Dempsey A.A. ;
Liew C.-C. .
Current Hypertension Reports, 1999, 1 (1) :51-58
[70]  
TOGGAS SM, 1992, MOL PHARMACOL, V42, P44