Mitochondria in Ca2+ signaling and apoptosis

Mitochondria in Ca2+ signaling and apoptosis

Autor Smaili, Soraya Soubhi Autor UNIFESP Google Scholar
Hsu, Y. T. Google Scholar
Youle, R. J. Google Scholar
Russell, J. T. Google Scholar
Instituição NICHHD
Universidade Federal de São Paulo (UNIFESP)
Resumo 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 Bar, 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.
Assunto Ca2+ signaling
inositol 1,4,5-trisphosphate receptor
mitochondrial Ca2+ uptake
mitochondrial Ca2+ efflux
permeability transition
Bcl-2 family
Idioma Inglês
Data 2000-02-01
Publicado em Journal of Bioenergetics and Biomembranes. New York: Kluwer Academic/plenum Publ, v. 32, n. 1, p. 35-46, 2000.
ISSN 0145-479X (Sherpa/Romeo, fator de impacto)
Editor Kluwer Academic/plenum Publ
Extensão 35-46
Direito de acesso Acesso restrito
Tipo Resenha
Web of Science WOS:000086629900005

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