Implications of Necroptosis for Cardiovascular Diseases

被引:37
作者
Ruan, Zhao-hui [1 ]
Xu, Zi-xuan [1 ]
Zhou, Xue-yun [1 ]
Zhang, Xian [1 ]
Shang, Lei [1 ]
机构
[1] Nanchang Univ, Affiliated Eye Hosp, Jiangxi Res Inst Ophthalmol & Visual Sci, Nanchang 330006, Jiangxi, Peoples R China
关键词
cell death; death-associated molecular patterns; necroptosis; cardiovascular disease; MIXED LINEAGE KINASE; LOW-DENSITY-LIPOPROTEIN; DOMAIN-LIKE PROTEIN; CELL-DEATH; PROGRAMMED NECROSIS; APOPTOSIS; RIP3; ATHEROSCLEROSIS; CARDIOMYOCYTES; INFLAMMATION;
D O I
10.1007/s11596-019-2067-6
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Necroptosis is a non-apoptotic programmed cell death pathway, which causes necrosis-like morphologic changes and triggers inflammation in the surrounding tissues. Accumulating evidence has demonstrated that necroptosis is involved in a number of pathological processes that lead to cardiovascular diseases. However, the exact molecular pathways linking them remain unknown. Herein, this review summarizes the necroptosis-related pathways involved in the development of various cardiovascular diseases, including atherosclerosis, cardiac ischemia-reperfusion injury, cardiac hypertrophy, dilated cardiomyopathy and myocardial infarction, and may shed light on the diagnosis and treatment of these diseases.
引用
收藏
页码:513 / 522
页数:10
相关论文
共 70 条
[1]   Cardiorespiratory Fitness and Cardiovascular Disease Prevention: an Update [J].
Al-Mallah, Mouaz H. ;
Sakr, Sherif ;
Al-Qunaibet, Ada .
CURRENT ATHEROSCLEROSIS REPORTS, 2018, 20 (01)
[2]   Sphingosine-1-phosphate is a missing cofactor for the E3 ubiquitin ligase TRAF2 [J].
Alvarez, Sergio E. ;
Harikumar, Kuzhuvelil B. ;
Hait, Nitai C. ;
Allegood, Jeremy ;
Strub, Graham M. ;
Kim, Eugene Y. ;
Maceyka, Michael ;
Jiang, Hualiang ;
Luo, Cheng ;
Kordula, Tomasz ;
Milstien, Sheldon ;
Spiegel, Sarah .
NATURE, 2010, 465 (7301) :1084-U149
[3]   cIAP1 and cIAP2 facilitate cancer cell survival by functioning as E3 ligases that promote RIP1 ubiquitination [J].
Bertrand, Mathieu J. M. ;
Milutinovic, Snezana ;
Dickson, Kathleen M. ;
Ho, Wai Chi ;
Boudreault, Alain ;
Durkin, Jon ;
Gillard, John W. ;
Jaquith, James B. ;
Morris, Stephen J. ;
Barker, Philip A. .
MOLECULAR CELL, 2008, 30 (06) :689-700
[4]  
Brunvand Harald, 2003, Tidsskr Nor Laegeforen, V123, P930
[5]  
Carden DL, 2000, J PATHOL, V190, P255, DOI 10.1002/(SICI)1096-9896(200002)190:3<255::AID-PATH526>3.0.CO
[6]  
2-6
[7]   Cardiac Specific Knockout of p53 Decreases ER Stress-Induced Mitochondrial Damage [J].
Chen, Qun ;
Thompson, Jeremy ;
Hu, Ying ;
Das, Anindita ;
Lesnefsky, Edward J. .
FRONTIERS IN CARDIOVASCULAR MEDICINE, 2019, 6
[8]   Translocation of mixed lineage kinase domain-like protein to plasma membrane leads to necrotic cell death [J].
Chen, Xin ;
Li, Wenjuan ;
Ren, Junming ;
Huang, Deli ;
He, Wan-ting ;
Song, Yunlong ;
Yang, Chao ;
Li, Wanyun ;
Zheng, Xinru ;
Chen, Pengda ;
Han, Jiahuai .
CELL RESEARCH, 2014, 24 (01) :105-121
[9]   Phosphorylation-Driven Assembly of the RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation [J].
Cho, YoungSik ;
Challa, Sreerupa ;
Moquin, David ;
Genga, Ryan ;
Ray, Tathagat Dutta ;
Guildford, Melissa ;
Chan, Francis Ka-Ming .
CELL, 2009, 137 (06) :1112-1123
[10]  
Dargel R, 1989, Z Med Lab Diagn, V30, P251