Cabassi Aderville, Miragoli Michele
Department of Medicine and Surgery, University of Parma, 43126 Parma, Italy.
Institute of Genetic and Biomedical Research, National Research Council, 20138 Milan, Italy.
Int J Mol Sci. 2017 Jul 10;18(7):1487. doi: 10.3390/ijms18071487.
The heart consists of millions of cells, namely cardiomyocytes, which are highly organized in terms of structure and function, at both macroscale and microscale levels. Such meticulous organization is imperative for assuring the physiological pump-function of the heart. One of the key players for the electrical and mechanical synchronization and contraction is the calcium ion via the well-known calcium-induced calcium release process. In cardiovascular diseases, the structural organization is lost, resulting in morphological, electrical, and metabolic remodeling owing the imbalance of the calcium handling and promoting heart failure and arrhythmias. Recently, attention has been focused on the role of mitochondria, which seem to jeopardize these events by misbalancing the calcium processes. In this review, we highlight our recent findings, especially the role of mitochondria (dys)function in failing cardiomyocytes with respect to the calcium machinery.
心脏由数百万个细胞组成，即心肌细胞，这些细胞在宏观和微观层面的结构和功能上都高度有序。这种精细的组织对于确保心脏的生理泵功能至关重要。钙离子通过著名的钙诱导钙释放过程，是实现电和机械同步及收缩的关键因素之一。在心血管疾病中，结构组织遭到破坏，由于钙处理失衡导致形态、电和代谢重塑，进而引发心力衰竭和心律失常。最近，人们的注意力集中在线粒体的作用上，线粒体似乎通过使钙过程失衡而危及这些事件。在本综述中，我们重点介绍我们最近的发现，特别是线粒体（功能障碍）在衰竭心肌细胞中相对于钙机制的作用。
