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Science 305 (5684): 626-629

Copyright © 2004 by the American Association for the Advancement of Science

The Pathophysiology of Mitochondrial Cell Death

Douglas R. Green1*, and Guido Kroemer2*

Abstract: In the mitochondrial pathway of apoptosis, caspase activation is closely linked to mitochondrial outer membrane permeabilization (MOMP). Numerous pro-apoptotic signal-transducing molecules and pathological stimuli converge on mitochondria to induce MOMP. The local regulation and execution of MOMP involve proteins from the Bcl-2 family, mitochondrial lipids, proteins that regulate bioenergetic metabolite flux, and putative components of the permeability transition pore. MOMP is lethal because it results in the release of caspase-activating molecules and caspase-independent death effectors, metabolic failure in the mitochondria, or both. Drugs designed to suppress excessive MOMP may avoid pathological cell death, and the therapeutic induction of MOMP may restore apoptosis in cancer cells in which it is disabled. The general rules governing the pathophysiology of MOMP and controversial issues regarding its regulation are discussed.

1 Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.
2 Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8125, Institut Gustave Roussy, 39 rue Camille-Desmoulins, F-94805 Villejuif, France.

* To whom correspondence should be addressed. E-mail: doug{at} (D.R.G.) and kroemer{at} (G.K.)

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Eukaryot. Cell 9, 906-914
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Global Targeting of Subcellular Heat Shock Protein-90 Networks for Therapy of Glioblastoma.
M. D. Siegelin, J. Plescia, C. M. Raskett, C. A. Gilbert, A. H. Ross, and D. C. Altieri (2010)
Mol. Cancer Ther. 9, 1638-1646
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Perturbation of the Bcl-2 Network and an Induced Noxa/Bcl-xL Interaction Trigger Mitochondrial Dysfunction after DNA Damage.
H. Lopez, L. Zhang, N. M. George, X. Liu, X. Pang, J. J. D. Evans, N. M. Targy, and X. Luo (2010)
J. Biol. Chem. 285, 15016-15026
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Manipulation of Death Pathways in Desmin-Related Cardiomyopathy.
A. Maloyan, J. Sayegh, H. Osinska, B. H. L. Chua, and J. Robbins (2010)
Circ. Res. 106, 1524-1532
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Involvement of Mitochondria-Mediated Apoptosis in Ethylbenzene-Induced Renal Toxicity in Rat.
M. Zhang, Y. Wang, Q. Wang, J. Yang, D. Yang, J. Liu, and J. Li (2010)
Toxicol. Sci. 115, 295-303
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Estrogen Receptor {beta} Agonism Increases Survival in Experimentally Induced Sepsis and Ameliorates the Genomic Sepsis Signature: A Pharmacogenomic Study.
E. Christaki, S. M. Opal, J. C. Keith Jr, N. Kessinian, J. E. Palardy, N. A. Parejo, E. Lavallie, L. Racie, W. Mounts, M. S. Malamas, et al. (2010)
The Journal of Infectious Disease 201, 1250-1257
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Mitochondrial DNA Toxicity in Forebrain Neurons Causes Apoptosis, Neurodegeneration, and Impaired Behavior.
K. H. Lauritzen, O. Moldestad, L. Eide, H. Carlsen, G. Nesse, J. F. Storm, I. M. Mansuy, L. H. Bergersen, and A. Klungland (2010)
Mol. Cell. Biol. 30, 1357-1367
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Up-Regulation of Histamine H4 Receptors Contributes to Splenic Apoptosis in Septic Mice: Counteraction of the Antiapoptotic Action of Nuclear Factor-{kappa}B.
N. Matsuda, H. Teramae, M. Futatsugi, K.-i. Takano, S. Yamamoto, K. Tomita, T. Suzuki, H. Yokoo, K. Koike, and Y. Hattori (2010)
J. Pharmacol. Exp. Ther. 332, 730-737
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Activities of SYK and PLC{gamma}2 Predict Apoptotic Response of CLL Cells to SRC Tyrosine Kinase Inhibitor Dasatinib.
Z. Song, P. Lu, R. R. Furman, J. P. Leonard, P. Martin, L. Tyrell, F. Y. Lee, D. M. Knowles, M. Coleman, and Y. L. Wang (2010)
Clin. Cancer Res. 16, 587-599
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Bax Contains Two Functional Mitochondrial Targeting Sequences and Translocates to Mitochondria in a Conformational Change- and Homo-oligomerization-driven Process.
N. M. George, N. Targy, J. J. D. Evans, L. Zhang, and X. Luo (2010)
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