Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling

Brazilian Journal of Medical and Biological Research

卷:36

关键词: Ca2+;    Mitochondrial Ca2+ uptake;    Mitochondrial Ca2+ efflux;    Permeability transition;    Apoptosis;    Bcl-2 family;    Bax and apoptosis;   

DOI  :  10.1590/S0100-879X2003000200004

来源: DOAJ

【 摘 要 】

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 (Dym). The collapse of Dym 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.

【 授权许可】

Unknown