Mitochondrial Reactive Oxygen Species at the Heart of the Matter New Therapeutic Approaches for Cardiovascular Diseases

被引:181
作者
Kornfeld, Opher S. [1 ]
Hwang, Sunhee [1 ]
Disatnik, Marie-HeLene [1 ]
Chen, Che-Hong [1 ]
Qvit, Nir [1 ]
Mochly-Rosen, Daria [1 ]
机构
[1] Stanford Univ, Sch Med, Dept Chem & Syst Biol, Stanford, CA 94305 USA
基金
美国国家卫生研究院;
关键词
mitochondria; mitochondrial degradation; mitochondrial dynamics; protein kinase C; reactive oxygen species; KINASE-C-DELTA; PERMEABILITY TRANSITION PORE; ISCHEMIA-REPERFUSION INJURY; ACUTE MYOCARDIAL-INFARCTION; PERCUTANEOUS CORONARY INTERVENTION; CONTRAST-INDUCED NEPHROPATHY; ALPHA-LIPOIC ACID; PKC-EPSILON; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; CARDIAC ISCHEMIA;
D O I
10.1161/CIRCRESAHA.116.305432
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Reactive oxygen species (ROS) have been implicated in a variety of age-related diseases, including multiple cardiovascular disorders. However, translation of ROS scavengers (antioxidants) into the clinic has not been successful. These antioxidants grossly reduce total levels of cellular ROS including ROS that participate in physiological signaling. In this review, we challenge the traditional antioxidant therapeutic approach that targets ROS directly with novel approaches that improve mitochondrial functions to more effectively treat cardiovascular diseases.
引用
收藏
页码:1783 / 1799
页数:17
相关论文
共 172 条
[1]   Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury [J].
Adlam, VJ ;
Harrison, JC ;
Porteous, CM ;
James, AM ;
Smith, RAJ ;
Murphy, MP ;
Sammut, IA .
FASEB JOURNAL, 2005, 19 (09) :1088-1095
[2]   Cyclophilin D and myocardial ischemia-reperfusion injury: A fresh perspective [J].
Alam, Muhammad Rizwan ;
Baetz, Delphine ;
Ovize, Michel .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2015, 78 :80-89
[3]   Mitochondria as a source and target of lipid peroxidation products in healthy and diseased heart [J].
Anderson, Ethan J. ;
Katunga, Lalage A. ;
Willis, Monte S. .
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 2012, 39 (02) :179-193
[4]   Mitophagy Is Required for Acute Cardioprotection by Simvastatin [J].
Andres, Allen M. ;
Hernandez, Genaro ;
Lee, Pamela ;
Huang, Chengqun ;
Ratliff, Eric P. ;
Sin, Jon ;
Thornton, Christine A. ;
Damasco, Marichris V. ;
Gottlieb, Roberta A. .
ANTIOXIDANTS & REDOX SIGNALING, 2014, 21 (14) :1960-1973
[5]   Effects of the mitochondria-targeted antioxidant SkQ1 on lifespan of rodents [J].
Anisimov, Vladimir N. ;
Egorov, Maxim V. ;
Krasilshchikova, Marina S. ;
Lyamzaev, Konstantin G. ;
Manskikh, Vasily N. ;
Moshkin, Mikhail P. ;
Novikov, Evgeny A. ;
Popovich, Irina G. ;
Rogovin, Konstantin A. ;
Shabalina, Irina G. ;
Shekarova, Olga N. ;
Skulachev, Maxim V. ;
Titova, Tatiana V. ;
Vygodin, Vladimir A. ;
Vyssokikh, Mikhail Yu. ;
Yurova, Maria N. ;
Zabezhinsky, Mark A. ;
Skulachev, Vladimir P. .
AGING-US, 2011, 3 (11) :1110-1119
[6]   BLOCKADE OF ISCHEMIC PRECONDITIONING IN DOGS BY THE NOVEL ATP DEPENDENT POTASSIUM CHANNEL ANTAGONIST SODIUM 5-HYDROXYDECANOATE [J].
AUCHAMPACH, JA ;
GROVER, GJ ;
GROSS, GJ .
CARDIOVASCULAR RESEARCH, 1992, 26 (11) :1054-1062
[7]  
Badalzadeh R, 2015, PERFUSION IN PRESS
[8]   Protein kinase Cε interacts with and inhibits the permeability transition pore in cardiac mitochondria [J].
Baines, CP ;
Song, CX ;
Zheng, YT ;
Wang, GW ;
Zhang, J ;
Wang, OL ;
Guo, Y ;
Bolli, R ;
Cardwell, EM ;
Ping, PP .
CIRCULATION RESEARCH, 2003, 92 (08) :873-880
[9]   Oxygen radicals released during ischemic preconditioning contribute to cardioprotection in the rabbit myocardium [J].
Baines, CP ;
Goto, M ;
Downey, JM .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1997, 29 (01) :207-216
[10]   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