Mitochondria in Ca2+ signaling and apoptosis

Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injury and programmed cell death; mitochondria play a pivotal role in the regulation of such cytosolic Ca2+ ([Ca2+]c) signals. Mitochondria are endowed with multiple Ca2+ transport mechanisms by which they take up...

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Bibliographic Details
Published in:Journal of bioenergetics and biomembranes 2000-02, Vol.32 (1), p.35-46
Main Authors: Smaili, S S, Hsu, Y T, Youle, R J, Russell, J T
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Calcium Signaling
Cell Death
Cellular biology
Intracellular Membranes - metabolism
Membranes
Mitochondria
Mitochondria - physiology
Mortality
Permeability
Proteins
Proto-Oncogene Proteins c-bcl-2 - metabolism
Translocation
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Summary:Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injury and programmed cell death; mitochondria play a pivotal role in the regulation of such cytosolic Ca2+ ([Ca2+]c) signals. Mitochondria are endowed with multiple Ca2+ transport mechanisms by which they take up and release Ca2+ across their inner membrane. These transport processes function to regulate local and global [Ca2+]c, thereby regulating a number of Ca2+-sensitive cellular mechanisms. The permeability transition pore (PTP) forms the major Ca2+ efflux pathway from mitochondria. In addition, Ca2+ efflux from the mitochondrial matrix occurs by the reversal of the uniporter and through the inner membrane Na+/Ca2+ exchanger. During cellular Ca2+ overload, mitochondria take up [Ca2+]c, which, in turn, induces opening of PTP, disruption of mitochondrial membrane potential (delta(psi)m) and cell death. In apoptosis signaling, collapse of delta(psi)m and cytochrome c release from mitochondria occur followed by activation of caspases, DNA fragmentation, and cell death. Translocation of Bax, an apoptotic signaling protein from the cytosol to the mitochondrial membrane, is another step during this apoptosis-signaling pathway. The role of permeability transition in the context of cell death in relation to Bcl-2 family of proteins is discussed.
ISSN:0145-479X
1573-6881
DOI:10.1023/A:1005508311495