Popoiu Tudor-Alexandru, Maack Christoph, Bertero Edoardo
Department of Translational Research, Comprehensive Heart Failure Center, University Clinic Würzburg, Würzburg, Germany.
"Victor Babes" University of Medicine and Pharmacy, Timisoara, Romania.
Front Mol Med. 2023 Aug 23;3:1235188. doi: 10.3389/fmmed.2023.1235188. eCollection 2023.
The energy demand of cardiomyocytes changes continuously in response to variations in cardiac workload. Cardiac excitation-contraction coupling is fueled primarily by adenosine triphosphate (ATP) production by oxidative phosphorylation in mitochondria. The rate of mitochondrial oxidative metabolism is matched to the rate of ATP consumption in the cytosol by the parallel activation of oxidative phosphorylation by calcium (Ca) and adenosine diphosphate (ADP). During cardiac workload transitions, Ca accumulates in the mitochondrial matrix, where it stimulates the activity of the tricarboxylic acid cycle. In this review, we describe how mitochondria internalize and extrude Ca, the relevance of this process for ATP production and redox homeostasis in the healthy heart, and how derangements in ion handling cause mitochondrial and cardiomyocyte dysfunction in heart failure.
心肌细胞的能量需求会随着心脏工作负荷的变化而持续改变。心脏兴奋 - 收缩偶联主要由线粒体中通过氧化磷酸化产生的三磷酸腺苷（ATP）提供能量。线粒体氧化代谢速率通过钙（Ca）和二磷酸腺苷（ADP）对氧化磷酸化的协同激活，与细胞质中ATP消耗速率相匹配。在心脏工作负荷转变期间，Ca在线粒体基质中积累，刺激三羧酸循环的活性。在本综述中，我们描述了线粒体如何摄取和排出Ca，该过程对健康心脏中ATP产生和氧化还原稳态的相关性，以及离子处理紊乱如何导致心力衰竭中的线粒体和心肌细胞功能障碍。
