Regulation of the Na+/Ca2+ Exchanger by Pyridine Nucleotide Redox Potential in Ventricular Myocytes

Liu, Ting; O’Rourke, Brian

doi:10.1074/jbc.m113.496588

Cited by 26 publications

(21 citation statements)

References 52 publications

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“…Figure adapted from ref. 42.j in maintaining mitochondrial antioxidant capacity (89,90). Higher levels of free Ca 2+ in the mitochondrial matrix in MyHC mutant mitochondria would be expected to stimulate ATP generation by OxPhos and could contribute to the reduced redox environment exhibited by isolated mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Allele-specific differences in transcriptome, miRNome, and mitochondrial function in two hypertrophic cardiomyopathy mouse models

Vakrou

Fukunaga²,

Foster

et al. 2018

JCI Insight

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Section: Discussionmentioning

confidence: 99%

Allele-specific differences in transcriptome, miRNome, and mitochondrial function in two hypertrophic cardiomyopathy mouse models

Vakrou

Fukunaga²,

Foster

et al. 2018

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“…There have been conflicting reports about ROS activating or inhibiting ion flux via NCX. 139, 140 Additional work is necessary to identify ROS-sensitive coactivators or related post-translational modifications. An analysis of potentially redox-sensitive cysteines failed to identify directly modified residues.…”

Section: Role Of Ros In Fundamental Cellular Responsesmentioning

confidence: 99%

Regulation of Signal Transduction by Reactive Oxygen Species in the Cardiovascular System

Brown

Griendling

2015

Circulation Research

414

310

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Oxidative stress has long been implicated in cardiovascular disease, but more recently, the role of reactive oxygen species in normal physiological signaling has been elucidated. Signaling pathways modulated by reactive oxygen species (ROS) are complex and compartmentalized, and we are only beginning to identify the molecular modifications of specific targets. Here we review the current literature regarding ROS signaling in the cardiovascular system, focusing on the role of ROS in normal physiology and how dysregulation of signaling circuits contributes to cardiovascular diseases including atherosclerosis, ischemia-reperfusion injury, cardiomyopathy and heart failure. In particular, we consider how ROS modulate signaling pathways related to phenotypic modulation, migration and adhesion, contractility, proliferation and hypertrophy, angiogenesis, endoplasmic reticulum stress, apoptosis and senescence. Understanding the specific targets of ROS may guide the development of the next generation of ROS-modifying therapies to reduce morbidity and mortality associated with oxidative stress.

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“…Concerning changes in myocardial cell membrane ion channel structure and function, ventricular electrical remodeling is an important cause of arrhythmia following myocardial infarction (Liu and O'Rourke, 2013;Bell et al, 2015). After myocardial infarction, reentry and "abnormal automaticity" are associated with ventricular arrhythmia.…”

Section: Discussionmentioning

confidence: 99%

Impact of citrate pretreatment on ventricular arrhythmia and myocardial capase-3 expression in ischemia/reperfusion injury

Lü¹,

Li²,

Zhou³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Ischemia/reperfusion (I/R) injury often triggers ventricular arrhythmia. Citrate binds calcium ions, forming a soluble calcium citrate complex that may reduce I/R injury by affecting calcium ion concentration. We tested the effects of citrate pretreatment on ventricular heart rate and related factors in a rat I/R model. Fifty male Sprague Dawley rats weighing 350-400 g were randomly divided into equally sized control (A), model (B), and 0.1 M (C), 0.05 M (D), and 0.025 M (E) citrate groups. An I/R model was established by ligating the left anterior descending coronary artery. Serum calcium ion concentration was measured before and after citrate treatment. Triphenyltetrazolium chloride staining and spectrophotometry were used to determine infarction area and caspase-3 protein levels in myocardial tissue, respectively. Polymerase chain reaction was performed to test myocardial calmodulin (CAM) expression. The frequency of ventricular arrhythmia in group B was significantly higher than in the sham surgery group (P < 0.05). Citrate pretreatment resulted in lower and higher frequencies than those observed in the model and control groups, respectively, in a dose-independent manner. The most obvious reduction in ventricular arrhythmia was seen in Group D. Serum calcium ion concentration decreased markedly after citrate treatment (P < 0.05), with a specific pattern emerging over time. Infarction area and caspase-3 and CAM levels were significantly lower in the citrate groups compared with the model group (P < 0.05). Citrate can reduce myocardial cell apoptosis, alleviating ventricular arrhythmia and protecting the myocardium by reducing serum calcium ion concentration and downregulating caspase-3 and CAM expression.

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Regulation of the Na+/Ca2+ Exchanger by Pyridine Nucleotide Redox Potential in Ventricular Myocytes

Cited by 26 publications

References 52 publications

Allele-specific differences in transcriptome, miRNome, and mitochondrial function in two hypertrophic cardiomyopathy mouse models

Allele-specific differences in transcriptome, miRNome, and mitochondrial function in two hypertrophic cardiomyopathy mouse models

Regulation of Signal Transduction by Reactive Oxygen Species in the Cardiovascular System

Impact of citrate pretreatment on ventricular arrhythmia and myocardial capase-3 expression in ischemia/reperfusion injury

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