Mitochondrial calcium in cardiac ischemia/reperfusion injury and cardioprotection.

IF 7.5 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Basic Research in Cardiology Pub Date : 2024-08-01 Epub Date: 2024-06-19 DOI:10.1007/s00395-024-01060-2
Edoardo Bertero, Tudor-Alexandru Popoiu, Christoph Maack
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Abstract

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.

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线粒体钙在心脏缺血/再灌注损伤和心脏保护中的作用。
线粒体钙(Ca2+)信号在心脏稳态和疾病中发挥着核心作用。在健康的心脏中,线粒体 Ca2+ 水平会调节氧化代谢速率,使之与细胞质中三磷酸腺苷的消耗速率相匹配。在缺血/再灌注(I/R)损伤期间,线粒体基质中病理性高水平的 Ca2+ 会触发线粒体通透性转换孔的打开,从而从基质中释放出溶质和小蛋白,引起线粒体肿胀,最终导致细胞死亡。通过调节主要 Ca2+ 流入和流出途径(即线粒体 Ca2+ 单通道和钠/Ca2+ 交换器)的活性来调整线粒体 Ca2+ 处理的药理和遗传方法,是保护心脏免受 I/R 损伤的有前途的治疗策略。
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来源期刊
Basic Research in Cardiology
Basic Research in Cardiology 医学-心血管系统
CiteScore
16.30
自引率
5.30%
发文量
54
审稿时长
6-12 weeks
期刊介绍: Basic Research in Cardiology is an international journal for cardiovascular research. It provides a forum for original and review articles related to experimental cardiology that meet its stringent scientific standards. Basic Research in Cardiology regularly receives articles from the fields of - Molecular and Cellular Biology - Biochemistry - Biophysics - Pharmacology - Physiology and Pathology - Clinical Cardiology
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