Smaili Soraya, Hirata Hanako, Ureshino Rodrigo, Monteforte Priscila T, Morales Ana P, Muler Mari L, Terashima Juliana, Oseki Karen, Rosenstock Tatiana R, Lopes Guiomar S, Bincoletto Claudia
Departamento de Farmacologia, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, SP, Brasil.
An Acad Bras Cienc. 2009 Sep;81(3):467-75. doi: 10.1590/s0001-37652009000300011.
Transient increase in cytosolic (Cac2+) and mitochondrial Ca2+ (Ca m2+) are essential elements in the control of many physiological processes. However, sustained increases in Ca c2+ and Ca m2+ may contribute to oxidative stress and cell death. Several events are related to the increase in Ca m2+, including regulation and activation of a number of Ca2+ dependent enzymes, such as phospholipases, proteases and nucleases. Mitochondria and endoplasmic reticulum (ER) play pivotal roles in the maintenance of intracellular Ca2+ homeostasis and regulation of cell death. Several lines of evidence have shown that, in the presence of some apoptotic stimuli, the activation of mitochondrial processes may lead to the release of cytochrome c followed by the activation of caspases, nuclear fragmentation and apoptotic cell death. The aim of this review was to show how changes in calcium signaling can be related to the apoptotic cell death induction. Calcium homeostasis was also shown to be an important mechanism involved in neurodegenerative and aging processes.
胞质（Ca c2+）和线粒体Ca2+（Ca m2+）的短暂增加是控制许多生理过程的关键因素。然而，Ca c2+和Ca m2+的持续增加可能导致氧化应激和细胞死亡。有几个事件与Ca m2+的增加有关，包括多种Ca2+依赖性酶的调节和激活，如磷脂酶、蛋白酶和核酸酶。线粒体和内质网（ER）在维持细胞内Ca2+稳态和调节细胞死亡方面起着关键作用。多项证据表明，在某些凋亡刺激存在的情况下，线粒体过程的激活可能导致细胞色素c的释放，随后激活半胱天冬酶、核碎片化和凋亡性细胞死亡。本综述的目的是展示钙信号的变化如何与凋亡性细胞死亡的诱导相关。钙稳态也被证明是参与神经退行性和衰老过程的重要机制。
