Washington University Center for Pharmacogenomics, Campus Box 8220, 660 S Euclid Ave, St Louis, MO 63110, USA.
Circ Res. 2010 Sep 17;107(6):689-99. doi: 10.1161/CIRCRESAHA.110.225714.
Mitochondria are key organelles in cell life whose dysfunction is associated with a variety of diseases. Their crucial role in intermediary metabolism and energy conversion makes them a preferred target in tissues, such as the heart, where the energetic demands are very high. In the cardiomyocyte, the spatial organization of mitochondria favors their interaction with the sarcoplasmic reticulum, thereby offering a mechanism for Ca(2+)-mediated crosstalk between these 2 organelles. Recently, the molecular basis for this interaction has begun to be unraveled, and we are learning how endoplasmic reticulum-mitochondrial interactions are often exploited by death signals, such as proapoptotic Bcl-2 family members, to amplify the cell death cascade. Here, we review our present understanding of the structural basis and the functional consequences of the close interaction between sarcoplasmic reticulum and mitochondria on cardiomyocyte function and death.
线粒体是细胞生命中的关键细胞器，其功能障碍与多种疾病有关。它们在中间代谢和能量转换中的关键作用使它们成为组织（如心脏）中的首选靶标，因为心脏的能量需求非常高。在心肌细胞中，线粒体的空间组织有利于它们与肌浆网的相互作用，从而为这两个细胞器之间的 Ca(2+)介导的串扰提供了一种机制。最近，这种相互作用的分子基础开始被揭示，我们也逐渐了解内质网-线粒体相互作用是如何被死亡信号（如促凋亡 Bcl-2 家族成员）利用来放大细胞死亡级联的。在这里，我们回顾了我们目前对肌浆网和线粒体之间紧密相互作用对心肌细胞功能和死亡的结构基础和功能后果的理解。
