Sarcoplasmic reticulum-mitochondria communication; implications for cardiac arrhythmia

被引:26
作者
Hamilton, Shanna [1 ]
Terentyeva, Radmila [1 ]
Clements, Richard T. [2 ]
Belevych, Andriy E. [1 ]
Terentyev, Dmitry [1 ]
机构
[1] Ohio State Univ, Dept Physiol & Cell Biol, Davis Heart & Lung Res Inst, Wexner Med Ctr, Columbus, OH 43210 USA
[2] Univ Rhode Isl, Biomed & Pharmaceut Sci, Kingston, RI 02881 USA
基金
美国国家卫生研究院;
关键词
Sarcoplasmic reticulum; Mitochondria; Calcium signaling; Cardiac arrhythmia; CA2+ UPTAKE; RYANODINE RECEPTOR; CALCIUM UNIPORTER; HEART-MITOCHONDRIA; REDOX MODIFICATION; OXIDATIVE STRESS; RYR2; ACTIVITY; CHANNELS; RELEASE; RABBIT;
D O I
10.1016/j.yjmcc.2021.04.002
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Sudden cardiac death due to ventricular tachyarrhythmias remains the major cause of mortality in the world. Heart failure, diabetic cardiomyopathy, old age-related cardiac dysfunction and inherited disorders are associated with enhanced propensity to malignant cardiac arrhythmias. Both defective mitochondrial function and abnormal intracellular Ca2+ homeostasis have been established as the key contributing factors in the pathophysiology and arrhythmogenesis in these conditions. This article reviews current advances in understanding of bidirectional control of ryanodine receptor-mediated sarcoplasmic reticulum Ca2+ release and mitochondrial function, and how defects in crosstalk between these two organelles increase arrhythmic risk in cardiac disease.
引用
收藏
页码:105 / 113
页数:9
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