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

Brazilian Journal of Medical and Biological Research

S.s. Smaili²  Y.-t. Hsu¹  A.c.p. Carvalho²  T.r. Rosenstock²  J.c. Sharpe¹  R.j. Youle¹ 

[1] ,Universidade Federal de São Paulo Escola Paulista de Medicina Instituto de FarmacologiaSão Paulo SP ,Brasil

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: SciELO

【 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】

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