De Nicolo Bianca, Cataldi-Stagetti Erica, Diquigiovanni Chiara, Bonora Elena
Department of Medical and Surgical Sciences, University of Bologna, 40138 Bologna, Italy.
Medical Genetics Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, 40138 Bologna, Italy.
Antioxidants (Basel). 2023 Feb 2;12(2):353. doi: 10.3390/antiox12020353.
Mitochondria are key players in energy production, critical activity for the smooth functioning of energy-demanding organs such as the muscles, brain, and heart. Therefore, dysregulation or alterations in mitochondrial bioenergetics primarily perturb these organs. Within the cell, mitochondria are the major site of reactive oxygen species (ROS) production through the activity of different enzymes since it is one of the organelles with the major availability of oxygen. ROS can act as signaling molecules in a number of different pathways by modulating calcium (Ca) signaling. Interactions among ROS and calcium signaling can be considered bidirectional, with ROS regulating cellular Ca signaling, whereas Ca signaling is essential for ROS production. In particular, we will discuss how alterations in the crosstalk between ROS and Ca can lead to mitochondrial bioenergetics dysfunctions and the consequent damage to tissues at high energy demand, such as the heart. Changes in Ca can induce mitochondrial alterations associated with reduced ATP production and increased production of ROS. These changes in Ca levels and ROS generation completely paralyze cardiac contractility. Thus, ROS can hinder the excitation-contraction coupling, inducing arrhythmias, hypertrophy, apoptosis, or necrosis of cardiac cells. These interplays in the cardiovascular system are the focus of this review.
线粒体是能量产生的关键参与者，对于肌肉、大脑和心脏等能量需求器官的平稳运作至关重要。因此，线粒体生物能量学的失调或改变主要会扰乱这些器官。在细胞内，线粒体是通过不同酶的活性产生活性氧（ROS）的主要场所，因为它是氧气供应充足的细胞器之一。ROS可以通过调节钙（Ca）信号在许多不同途径中充当信号分子。ROS与钙信号之间的相互作用可以被认为是双向的，ROS调节细胞内钙信号，而钙信号对于ROS的产生至关重要。特别是，我们将讨论ROS与Ca之间的串扰改变如何导致线粒体生物能量学功能障碍以及随之而来的对高能量需求组织（如心脏）的损伤。Ca的变化可诱导与ATP生成减少和ROS生成增加相关的线粒体改变。Ca水平和ROS生成的这些变化会完全使心脏收缩力瘫痪。因此，ROS会阻碍兴奋 - 收缩偶联，诱发心律失常、心肌肥大、细胞凋亡或坏死。心血管系统中的这些相互作用是本综述的重点。
