Mitochondrial calcium (Ca²⁺) signals play a central role in cardiac homeostasis and disease. In the healthy heart, mitochondrial Ca²⁺ levels modulate the rate of oxidative metabolism to match the rate of adenosine triphosphate consumption in the cytosol. During ischemia/reperfusion (I/R) injury, pathologically high levels of Ca²⁺ in the mitochondrial matrix trigger the opening of the mitochondrial permeability transition pore, which releases solutes and small proteins from the matrix, causing mitochondrial swelling and ultimately leading to cell death. Pharmacological and genetic approaches to tune mitochondrial Ca²⁺ handling by regulating the activity of the main Ca²⁺ influx and efflux pathways, i.e., the mitochondrial Ca²⁺ uniporter and sodium/Ca²⁺ exchanger, represent promising therapeutic strategies to protect the heart from I/R injury.

线粒体钙 （Ca²⁺） 信号在心脏稳态和疾病中起着核心作用。在健康的心脏中，线粒体 Ca²⁺ 水平调节氧化代谢速率，以匹配胞质溶胶中三磷酸腺苷的消耗速率。在缺血/再灌注 （I/R） 损伤期间，线粒体基质中病理上高水平的 Ca²⁺ 触发线粒体通透性转换孔的打开，从而从基质中释放溶质和小蛋白，导致线粒体肿胀并最终导致细胞死亡。通过调节主要 Ca²⁺ 内流和外排途径（即线粒体 Ca²⁺ 单向转运蛋白和钠/Ca²⁺ 交换剂）的活性来调节线粒体 Ca²⁺ 处理的药理学和遗传学方法，代表了保护心脏免受 I/R 损伤的有前途的治疗策略。