Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injury and programmed cell death through the regulation of a number of Ca2+-dependent enzymes such as phospholipases, proteases, and nucleases. Mitochondria along with the endoplasmic reticulum play pivotal roles in regulating intracellular Ca2+ content. Mitochondria are endowed with multiple Ca2+ transport mechanisms by which they take up and release Ca2+ across their inner membrane. During cellular Ca2+ overload, mitochondria take up cytosolic Ca2+, which in turn induces opening of permeability transition pores and disrupts the mitochondrial membrane potential (ΔΨm). The collapse of ΔΨm along with the release of cytochrome c from mitochondria is followed by the activation of caspases, nuclear fragmentation and cell death. Members of the Bcl-2 family are a group of proteins that play important roles in apoptosis regulation. Members of this family appear to differentially regulate intracellular Ca2+ level. Translocation of Bax, an apoptotic signaling protein, from the cytosol to the mitochondrial membrane is another step in this apoptosis signaling pathway.
CITATION STYLE
Smaili, S. S., Hsu, T. T., Carvalho, A. C. P., Rosenstock, T. R., Sharpe, J. C., & Youle, R. J. (2003, February 1). Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling. Brazilian Journal of Medical and Biological Research. Associacao Brasileira de Divulgacao Cientifica. https://doi.org/10.1590/S0100-879X2003000200004
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