Department of Physiology and Cellular Biophysics, Clyde and Helen Wu Center for Molecular Cardiology, Columbia University Vagelos College of Physicians & Surgeons, New York, NY 10032, USA.
Department of Medicine, Division of Cardiology, Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, New York, NY 10461, USA.
Biomolecules. 2023 Sep 19;13(9):1409. doi: 10.3390/biom13091409.
Heart failure is a serious global health challenge, affecting more than 6.2 million people in the United States and is projected to reach over 8 million by 2030. Independent of etiology, failing hearts share common features, including defective calcium (Ca) handling, mitochondrial Ca overload, and oxidative stress. In cardiomyocytes, Ca not only regulates excitation-contraction coupling, but also mitochondrial metabolism and oxidative stress signaling, thereby controlling the function and actual destiny of the cell. Understanding the mechanisms of mitochondrial Ca uptake and the molecular pathways involved in the regulation of increased mitochondrial Ca influx is an ongoing challenge in order to identify novel therapeutic targets to alleviate the burden of heart failure. In this review, we discuss the mechanisms underlying altered mitochondrial Ca handling in heart failure and the potential therapeutic strategies.
心力衰竭是一个严重的全球健康挑战，影响了美国超过 620 万人，预计到 2030 年将达到 800 多万人。无论病因如何，衰竭的心脏都有一些共同的特征，包括钙（Ca）处理缺陷、线粒体 Ca 过载和氧化应激。在心肌细胞中，Ca 不仅调节兴奋-收缩偶联，还调节线粒体代谢和氧化应激信号，从而控制细胞的功能和实际命运。为了确定减轻心力衰竭负担的新的治疗靶点，了解线粒体 Ca 摄取的机制以及调节增加的线粒体 Ca 内流的分子途径仍然是一个挑战。在这篇综述中，我们讨论了心力衰竭中线粒体 Ca 处理改变的机制以及潜在的治疗策略。
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