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Science 30 July 2004:
Vol. 305. no. 5684, pp. 626 - 629
DOI: 10.1126/science.1099320
Prev | Table of Contents | Next

Review

The Pathophysiology of Mitochondrial Cell Death

Douglas R. Green1* and Guido Kroemer2*

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}liai.org (D.R.G.) and kroemer{at}igr.fr (G.K.)

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Restoration of Tissue Factor Pathway Inhibitor-2 in a Human Glioblastoma Cell Line Triggers Caspase-Mediated Pathway and Apoptosis.
J. George, C. S. Gondi, D. H. Dinh, M. Gujrati, and J. S. Rao (2007)
Clin. Cancer Res. 13, 3507-3517
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Inhibition of ubiquitin-mediated degradation of MOAP-1 by apoptotic stimuli promotes Bax function in mitochondria.
N. Y. Fu, S. K. Sukumaran, and V. C. Yu (2007)
PNAS 104, 10051-10056
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Complex I Binding by a Virally Encoded RNA Regulates Mitochondria-Induced Cell Death.
M. B. Reeves, A. A. Davies, B. P. McSharry, G. W. Wilkinson, and J. H. Sinclair (2007)
Science 316, 1345-1348
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Functional Linkage between NOXA and Bim in Mitochondrial Apoptotic Events.
J. Han, L. A. Goldstein, W. Hou, and H. Rabinowich (2007)
J. Biol. Chem. 282, 16223-16231
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Assessment of Severity of Coronary Artery Stenosis in a Canine Model Using the PET Agent 18F-Fluorobenzyl Triphenyl Phosphonium: Comparison with 99mTc-Tetrofosmin.
I. Madar, H. Ravert, A. DiPaula, Y. Du, R. F. Dannals, and L. Becker (2007)
J. Nucl. Med. 48, 1021-1030
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Honokiol Induces a Necrotic Cell Death through the Mitochondrial Permeability Transition Pore.
L. Li, W. Han, Y. Gu, S. Qiu, Q. Lu, J. Jin, J. Luo, and X. Hu (2007)
Cancer Res. 67, 4894-4903
   Abstract »    Full Text »    PDF »
Caspase-9 regulates apoptosis/proliferation balance during metamorphic brain remodeling in Xenopus.
L. Coen, K. Le Blay, I. Rowe, and B. A. Demeneix (2007)
PNAS 104, 8502-8507
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Deficiency of Bim in dendritic cells contributes to overactivation of lymphocytes and autoimmunity.
M. Chen, L. Huang, and J. Wang (2007)
Blood 109, 4360-4367
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Cyanidin-3-rutinoside, a Natural Polyphenol Antioxidant, Selectively Kills Leukemic Cells by Induction of Oxidative Stress.
R. Feng, H.-M. Ni, S. Y. Wang, I. L. Tourkova, M. R. Shurin, H. Harada, and X.-M. Yin (2007)
J. Biol. Chem. 282, 13468-13476
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Bax Is Activated during Rotavirus-Induced Apoptosis through the Mitochondrial Pathway.
S. Martin-Latil, L. Mousson, A. Autret, F. Colbere-Garapin, and B. Blondel (2007)
J. Virol. 81, 4457-4464
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Aloe vera leaf exudate induces a caspase-independent cell death in Leishmania donovani promastigotes.
A. Dutta, S. Bandyopadhyay, C. Mandal, and M. Chatterjee (2007)
J. Med. Microbiol. 56, 629-636
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