Potential Therapeutic Benefits of Strategies Directed to Mitochondria

被引:143
作者
Camara, Amadou K. S. [1 ]
Lesnefsky, Edward J. [5 ,6 ,7 ]
Stowe, David F. [1 ,2 ,3 ,4 ]
机构
[1] Med Coll Wisconsin, Dept Anesthesiol, Milwaukee, WI 53226 USA
[2] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA
[3] Med Coll Wisconsin, Cardiovasc Res Ctr, Milwaukee, WI 53226 USA
[4] Vet Affairs Med Ctr, Res Serv, Milwaukee, WI USA
[5] Hunter Holmes McGuire Vet Affairs Med Ctr, Med Serv, Richmond, VA USA
[6] Virginia Commonwealth Univ, Dept Med, Div Cardiol, Richmond, VA 23298 USA
[7] Virginia Commonwealth Univ, Dept Biochem, Div Cardiol, Richmond, VA USA
基金
美国国家卫生研究院;
关键词
PERMEABILITY TRANSITION PORE; MANGANESE SUPEROXIDE-DISMUTASE; ISCHEMIA-REPERFUSION INJURY; AMYLOID-BETA-PEPTIDE; OXIDOREDUCTASE COMPLEX-I; TYPE-2; DIABETES-MELLITUS; DEPENDENT ANION CHANNEL; NITRIC-OXIDE SYNTHASE; KINASE-C-EPSILON; K-ATP CHANNELS;
D O I
10.1089/ars.2009.2788
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The mitochondrion is the most important organelle in determining continued cell survival and cell death. Mitochondrial dysfunction leads to many human maladies, including cardiovascular diseases, neurodegenerative disease, and cancer. These mitochondria-related pathologies range from early infancy to senescence. The central premise of this review is that if mitochondrial abnormalities contribute to the pathological state, alleviating the mitochondrial dysfunction would contribute to attenuating the severity or progression of the disease. Therefore, this review will examine the role of mitochondria in the etiology and progression of several diseases and explore potential therapeutic benefits of targeting mitochondria in mitigating the disease processes. Indeed, recent advances in mitochondrial biology have led to selective targeting of drugs designed to modulate and manipulate mitochondrial function and genomics for therapeutic benefit. These approaches to treat mitochondrial dysfunction rationally could lead to selective protection of cells in different tissues and various disease states. However, most of these approaches are in their infancy. Antioxid. Redox Signal. 13, 279-347.
引用
收藏
页码:279 / 347
页数:69
相关论文
共 658 条
  • [1] Cardioprotective effect of ischemic preconditioning is preserved in food-restricted senescent rats
    Abete, P
    Testa, G
    Ferrara, N
    De Santis, D
    Capaccio, P
    Viati, L
    Calabrese, C
    Cacciatore, F
    Longobardi, G
    Condorelli, M
    Napoli, C
    Rengo, F
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2002, 282 (06): : H1978 - H1987
  • [2] Hexokinase-I protection against apoptotic cell death is mediated via interaction with the voltage-dependent anion channel-1 - Mapping the site of binding
    Abu-Hamad, Salah
    Zaid, Hilal
    Israelson, Adrian
    Nahon, Edna
    Shoshan-Barmatz, Varda
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2008, 283 (19) : 13482 - 13490
  • [3] Bcl-2-regulated apoptosis: mechanism and therapeutic potential
    Adams, Jerry M.
    Cory, Suzanne
    [J]. CURRENT OPINION IN IMMUNOLOGY, 2007, 19 (05) : 488 - 496
  • [4] The Bcl-2 protein family: Arbiters of cell survival
    Adams, JM
    Cory, S
    [J]. SCIENCE, 1998, 281 (5381) : 1322 - 1326
  • [5] Apoptosis-associated release of Smac/DIABLO from mitochondria requires active caspases and is blocked by Bcl-2
    Adrain, C
    Creagh, EM
    Martin, SJ
    [J]. EMBO JOURNAL, 2001, 20 (23) : 6627 - 6636
  • [6] Mutant SOD1 from spinal cord of G93A rats is destabilized and binds to inner mitochondrial membrane
    Ahtoniemi, Toni
    Jaronen, Merja
    Keksa-Goldsteine, Velta
    Goldsteins, Gundars
    Koistinaho, Jari
    [J]. NEUROBIOLOGY OF DISEASE, 2008, 32 (03) : 479 - 485
  • [7] Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release
    Aidakkak, Mohammed
    Stowe, David F.
    Chen, Qun
    Lesnefsky, Edward J.
    Camara, Amadou K. S.
    [J]. CARDIOVASCULAR RESEARCH, 2008, 77 (02) : 406 - 415
  • [8] ALDAKKAK M, 2009, FASEB J, V793
  • [9] ALDAKKAK M, 2008, J BIOPHYSICS
  • [10] ALDAKKAK M, 2008, FASEB J, V730