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胞质Ca2 + 升高是细胞凋亡中Ca2 + 调节的经典模式 ,但近年来有证据表明胞质Ca2 + 下降同样能诱导细胞凋亡。目前研究发现 ,胞内Ca2 + 在细胞质、细胞核以及细胞钙库线粒体和内质网的动态平衡破坏和重新分布直接参与细胞凋亡信号的调控 ,而Bcl 2家族蛋白在细胞凋亡过程的胞内Ca2 + 调节及继后的一系列生理效应中发挥特殊作用。细胞凋亡中Ca2 + 调节的深入研究不但有助于阐明细胞凋亡的调控机理 ,同时为相关疾病防治和药物开发提供新的策略
Cytoplasmic Ca2 + is a classic model of Ca2 + regulation in apoptosis, but in recent years there is evidence that cytoplasmic Ca2 + decline can also induce apoptosis. The present study found that intracellular Ca2 + in the cytoplasm, nucleus and cellular calcium pool mitochondrial and endoplasmic reticulum dynamic balance of damage directly involved in the regulation of apoptosis signals, and Bcl2 family proteins in the process of apoptosis Ca2 + regulation and subsequent series of physiological effects play a special role. In-depth study of Ca2 + regulation in apoptosis not only helps clarify the regulatory mechanism of apoptosis, but also provides a new strategy for the prevention and treatment of related diseases and drug development