Targeting Mitochondria for Cardiac Protection

被引：28

作者：

Hernandez-Resendiz, Sauri ^{[1
]}

Buelna-Chontal, Mabel ^{[1
,2
]}

Correa, Francisco ^{[1
,2
]}

Zazueta, Cecilia ^{[1
,2
]}

机构：

[1] Natl Inst Cardiol Ignacio Chavez, Dept Biochem, Mexico City 14080, DF, Mexico

[2] Natl Inst Cardiol Ignacio Chavez, Dept Cardiovasc Biomed, Mexico City 14080, DF, Mexico

来源：

CURRENT DRUG TARGETS | 2013年 / 14卷 / 05期

关键词：

Apoptosis; cardioprotection; fusion and fission processes; mitochondrial biogenesis; mitochondrial calcium transport; oxidative stress; PERMEABILITY TRANSITION PORE; NECROSIS-FACTOR-ALPHA; REDUCES INFARCT SIZE; KINASE-C-EPSILON; K-ATP CHANNELS; ISCHEMIA-REPERFUSION; HEART-FAILURE; CYCLOSPORINE-A; OXIDATIVE STRESS; INNER MEMBRANE;

D O I：

10.2174/1389450111314050008

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The critical role of mitochondria in cardiomyocyte survival and death has become an exciting field of research in cardiac biology. Indeed, it is accepted that mitochondrial dysfunction plays a crucial role in the pathogenesis of multiple cardiac diseases. Besides the obvious relevance of mitochondria in energy production, calcium homeostasis, and reactive oxygen species (ROS) production, new processes like mitochondrial fusion/fission, phosphorylation and nitrosylation modifications in mitochondrial proteins have been suggested to form part of a cast of key players in cardiac disease. This review describes currently studied drugs and compounds that target mitochondria in the scenario of cardiovascular diseases.

引用

页码：586 / 600

页数：15

共 186 条

[1] Interplay between Ca2+ cycling and mitochondrial permeability transition pores promotes reperfusion-induced injury of cardiac myocytes [J].

Abdallah, Yaser ;

Kasseckert, Sascha A. ;

Iraqi, Wisam ;

Said, Maher ;

Shahzad, Tayyab ;

Erdogan, Ali ;

Neuhof, Christiane ;

Guenduez, Duersuen ;

Schlueter, Klaus-Dieter ;

Tillmanns, Harald ;

Piper, H. Michael ;

Reusch, H. Peter ;

Ladilov, Yury .

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2011, 15 (11) :2478-2485

[2] 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

[3] The mitochondrial origin of postischernic arrhythmias [J].

Akar, FG ;

Aon, MA ;

Tomaselli, GF ;

O'Rourke, B .

JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (12) :3527-3535

[4] Ceramide in the antiapoptotic effect of ischemic preconditioning [J].

Argaud, L ;

Prigent, AF ;

Chalabreysse, L ;

Loufouat, J ;

Lagarde, M ;

Ovize, M .

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2004, 286 (01) :H246-H251

[5] IMPAIRMENT BY CYCLOSPORINE-A OF REPERFUSION-INDUCED ARRHYTHMIAS [J].

ARTEAGA, D ;

ODOR, A ;

LOPEZ, RM ;

CONTRERAS, G ;

PICHARDO, J ;

GARCIA, E ;

ARANDA, A ;

CHAVEZ, E .

LIFE SCIENCES, 1992, 51 (14) :1127-1134

[6] Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death [J].

Baines, Christopher P. ;

Kaiser, Robert A. ;

Sheiko, Tatiana ;

Craigen, William J. ;

Molkentin, Jeffery D. .

NATURE CELL BIOLOGY, 2007, 9 (05) :550-U122

[7] 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

[8] Anti-tumour necrosis factor-α therapy in heart failure:: Future directions [J].

Balakumar, Pitchai ;

Singh, Manjeet .

BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY, 2006, 99 (06) :391-397

[9] OPA1 cleavage depends on decreased mitochondrial ATP level and bivalent metals [J].

Baricault, Laurent ;

Segui, Bruno ;

Guegand, Laurie ;

Olichon, Aurelien ;

Valette, Annie ;

Larminat, Florence ;

Lenaers, Guy .

EXPERIMENTAL CELL RESEARCH, 2007, 313 (17) :3800-3808

[10] Activation of peroxisome proliferator-activated receptor pathway stimulates the mitochondrial respiratory chain and can correct deficiencies in patients' cells lacking its components [J].

Bastin, Jean ;

Aubey, Flore ;

Rotig, Agnes ;

Munnich, Arnold ;

Djouadi, Fatima .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2008, 93 (04) :1433-1441

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