英凋亡中线粒体的作用.doc

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英凋亡中线粒体的作用

Mitochondria in Apoptosis and Human Disease M. Olson and S. Kornbluth* Department of Pharmacology and Cancer Biology Duke University Medical Center Durham, NC 27110, USA ? *Address correspondence to this authors at the Department of Pharmacology and Cancer Biology Duke University Medical Center Durham, NC 27110, USA; Fax: +1-919-613-8625 ? Abstract: Apoptosis is a process of cell suicide whereby individual cells are destroyed while preserving the integrity and architecture of surrounding tissue. This targeted cell destruction is critical both in physiological contexts as well as pathological states. It seems increasingly evident that mitochondria play an important role in the regulation of programmed cell death via release of proapoptotic agents and/or disruption of cellular energy metabolism. The mechanisms of mitochondrial involvement are beginning to be elucidated, and may involve the participation of bcl-2 family members, reactive oxygen species, and caspases. As part of a central mechanism of amplification of the apoptotic signal, mitochondria may be an appropriate target for therapeutic agents designed to modulate apoptosis. This review focuses on recent advances in understanding mitochondrial mechanisms in apoptosis and the involvement of these pathways in human disease. ? Introduction Apoptosis, or programmed cell death, is a cellular suicide program in which individual cells are destroyed while the integrity and architecture of surrounding tissue is preserved. This targeted cell destruction is critical in many physiological contexts including embryogenesis, immune cell maturation and response, tissue homeostasis, and in the cellular response to injury. Apoptosis (or lack thereof) is also important in several pathological states: excessive or inappropriate apoptosis has been implicated in immunodeficiencies (e.g. AIDS), Alzheimer’s disease and Parkinson’s disease, among others (reviewed in [1], [2]), while a failure of cells to die appropriately almost c

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