PDF(Pubmed)
Abstract：
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 (Ca2+) handling, mitochondrial Ca2+ overload, and oxidative stress. In cardiomyocytes, Ca2+ 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 Ca2+ uptake and the molecular pathways involved in the regulation of increased mitochondrial Ca2+ 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 Ca2+ handling in heart failure and the potential therapeutic strategies.
摘要：
心力衰竭是一个严重的全球性健康挑战，影响美国超过620万人，预计到2030年将达到800万人。独立于病因，失败的心具有共同的特征，包括有缺陷的钙（Ca2+）处理，线粒体Ca2+过载，和氧化应激。在心肌细胞中，Ca2+不仅调节激发-收缩耦合，还有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。了解线粒体Ca2+摄取的机制和参与调节增加的线粒体Ca2+流入的分子途径是一个持续的挑战，以确定新的治疗靶标来减轻心力衰竭的负担。在这次审查中,我们讨论了心力衰竭中线粒体Ca2+处理改变的潜在机制和潜在的治疗策略。
