Mitochondria are highly dynamic organelles extremely important for cell survival. Their structure resembles that of prokaryotic cells since they are composed with two membranes, the inner (IMM) and the outer mitochondrial membrane (OMM) delimitating the intermembrane space (IMS) and the matrix which contains mitochondrial DNA (mtDNA). This structure is strictly related to mitochondrial function since they produce the most of the cellular ATP through the oxidative phosphorylation which generate the electrochemical gradient at the two sides of the inner mitochondrial membrane an essential requirement for mitochondrial function. Cells of highly metabolic demand like those composing muscle, liver and brain, are particularly dependent on mitochondria for their activities. Mitochondria undergo to continual changes in morphology since, they fuse and divide, branch and fragment, swell and extend. Importantly, they move throughout the cell to deliver ATP and other metabolites where they are mostly required. Along with the capability to control energy metabolism, mitochondria play a critical role in the regulation of many physiological processes such as programmed cell death, autophagy, redox signalling, and stem cells reprogramming. All these phenomena are regulated by Ca²⁺ ions within this organelle. This review will discuss the molecular mechanisms regulating mitochondrial calcium cycling in physiological and pathological conditions with particular regard to their impact on mitochondrial dynamics and function during ischemia. Particular emphasis will be devoted to the role played by NCX3 and AKAP121 as new molecular targets for mitochondrial function and dysfunction.

线粒体是高度动态的细胞器，对于细胞存活极为重要。它们的结构类似于原核细胞，因为它们由两层膜组成，内膜（IMM）和线粒体外膜（OMM）界定了膜间空间（IMS）和包含线粒体DNA（mtDNA）的基质。这种结构与线粒体功能严格相关，因为它们通过氧化磷酸化产生大部分细胞ATP，这在线粒体内膜的两侧产生电化学梯度，这是线粒体功能的基本要求。诸如组成肌肉，肝脏和大脑的那些具有高代谢需求的细胞的活动特别依赖于线粒体。线粒体不断发生形态变化，因为，它们融合并分裂，分支并破碎，膨胀并延伸。重要的是，它们在整个细胞中移动，以在最需要它们的地方传递ATP和其他代谢产物。线粒体不仅具有控制能量代谢的能力，而且在调节许多生理过程（例如程序性细胞死亡，自噬，氧化还原信号和干细胞重编程）中起着至关重要的作用。所有这些现象都受钙的调节该细胞器中有^2+个离子。这篇综述将讨论在生理和病理条件下调节线粒体钙循环的分子机制，特别是它们对缺血过程中线粒体动力学和功能的影响。特别强调NCX3和AKAP121作为线粒体功能和功能障碍的新分子靶标所起的作用。