ER stress in cardiovascular disease

被引:299
作者
Minamino, Tetsuo [1 ]
Kitakaze, Masafumi [2 ]
机构
[1] Osaka Univ, Dept Cardiovasc Med, Grad Sch Med, Suita, Osaka 5650871, Japan
[2] Natl Cardiovasc Ctr, Dept Cardiovasc Med, Osaka 5658565, Japan
关键词
Endoplasmic reticulum; ER stress; Heart failure; Anti-cancer drug; Atherosclerosis; Plaque rupture; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED-PROTEIN RESPONSE; ATTENUATES CARDIOMYOCYTE DEATH; CELL-DEATH; ISCHEMIA/REPERFUSION INJURY; TARGETED DELETION; INDUCED APOPTOSIS; CARDIAC MYOCYTES; TRANSGENIC MICE; ACTIVATION;
D O I
10.1016/j.yjmcc.2009.10.026
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The endoplasmic reticulum (ER) is an organelle involved in protein folding, calcium homeostasis, and lipid biosynthesis. Various factors that interfere with ER function lead to accumulation of unfolded proteins, including oxidative stress, ischemia, disturbance of calcium homeostasis, and overexpression of normal and/or incorrectly folded proteins. The resulting ER stress triggers the unfolded protein response (UPR) that induces signal transduction events to reduce the accumulation of unfolded proteins by increasing ER resident chaperones, inhibiting protein translation, and accelerating the degradation of unfolded proteins. However, if stress is severe and/or prolonged, the ER also initiates apoptotic signaling that includes induction of the proapoptotic transcriptional factor C/EBP homologous protein, activation of c-Jun amino-terminal kinase, and cleavage of caspase-12. These ER-initiated events lead to cell death via mitochondria-dependent and-independent apoptotic pathways. Furthermore, the B cell lymphoma 2 family of proteins expressed on the ER and mitochondria are also involved in regulating cell death due to ER stress. Thus, the ER is now recognized as a vitally important organelle that can decide cell survival or death. Recent animal and human studies have revealed that the UPR and ER-initiated apoptosis are implicated in the pathophysiology of various cardiovascular diseases, including heart failure, ischemic heart disease, the development of atherosclerosis, and plaque rupture. Improved understanding of the molecular mechanisms underlying UPR activation and ER-initiated apoptosis in cardiovascular disease will provide us with new targets for drug discovery and therapeutic intervention. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1105 / 1110
页数:6
相关论文
共 55 条
[1]   XBP1 controls diverse cell type- and condition-specific transcriptional regulatory networks [J].
Acosta-Alvear, Diego ;
Zhou, Yiming ;
Blais, Alexandre ;
Tsikitis, Mary ;
Lents, Nathan H. ;
Arias, Carolina ;
Lennon, Christen J. ;
Kluger, Yuval ;
Dynlacht, Brian David .
MOLECULAR CELL, 2007, 27 (01) :53-66
[2]   Calcium cycling and signaling in cardiac myocytes [J].
Bers, Donald M. .
ANNUAL REVIEW OF PHYSIOLOGY, 2008, 70 :23-49
[3]   Dynamic interaction of BiP and ER stress transducers in the unfolded-protein response [J].
Bertolotti, A ;
Zhang, YH ;
Hendershot, LM ;
Harding, HP ;
Ron, D .
NATURE CELL BIOLOGY, 2000, 2 (06) :326-332
[4]   Compartmentalized expression of three novel sarco/endoplasmic reticulum Ca2+ATPase 3 isoforms including the switch to ER stress, SERCA3f, in non-failing and failing human heart [J].
Dally, Saoussen ;
Monceau, Virginie ;
Corvazier, Elisabeth ;
Bredoux, Raymonde ;
Raies, Aly ;
Bobe, Regis ;
del Monte, Federica ;
Enouf, Jocelyne .
CELL CALCIUM, 2009, 45 (02) :144-154
[5]   Endoplasmic reticulum-mitochondria crosstalk in NIX-mediated murine cell death [J].
Diwan, Abhinav ;
Matkovich, Scot J. ;
Yuan, Qunying ;
Zhao, Wen ;
Yatani, Atsuko ;
Brown, Joan Heller ;
Molkentin, Jeffery D. ;
Kranias, Evangelia G. ;
Dorn, Gerald W., II .
JOURNAL OF CLINICAL INVESTIGATION, 2009, 119 (01) :203-212
[6]   The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages [J].
Feng, B ;
Yao, PM ;
Li, YK ;
Devlin, CM ;
Zhang, DJ ;
Harding, HP ;
Sweeney, M ;
Rong, JX ;
Kuriakose, G ;
Fisher, EA ;
Marks, AR ;
Ron, D ;
Tabas, I .
NATURE CELL BIOLOGY, 2003, 5 (09) :781-792
[7]   Cardiotoxicity of the new cancer therapeutics -: mechanisms of, and approaches to, the problem [J].
Force, Thomas ;
Kerkelae, Risto .
DRUG DISCOVERY TODAY, 2008, 13 (17-18) :778-784
[8]   Overexpression of endoplasmic reticulum-resident chaperone attenuates cardiomyocyte death induced by proteasome inhibition [J].
Fu, Hai Ying ;
Minamino, Tetsuo ;
Tsukamoto, Osamu ;
Sawada, Tamaki ;
Asai, Mitsutoshi ;
Kato, Hisakazu ;
Asano, Yoshihiro ;
Fujita, Masashi ;
Takashima, Seiji ;
Hori, Masatsugu ;
Kitakaze, Masafumi .
CARDIOVASCULAR RESEARCH, 2008, 79 (04) :600-610
[9]   Global analysis of protein expression in yeast [J].
Ghaemmaghami, S ;
Huh, W ;
Bower, K ;
Howson, RW ;
Belle, A ;
Dephoure, N ;
O'Shea, EK ;
Weissman, JS .
NATURE, 2003, 425 (6959) :737-741
[10]   Dilated cardiomyopathy caused by aberrant endoplasmic reticulum quality control in mutant KDEL receptor transgenic mice [J].
Hamada, H ;
Suzuki, M ;
Yuasa, S ;
Mimura, N ;
Shinozuka, N ;
Takada, Y ;
Suzuki, M ;
Nishino, T ;
Nakaya, H ;
Koseki, H ;
Aoe, T .
MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (18) :8007-8017