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连接蛋白43与心肌缺血-再灌注损伤

Connexin43 and Myocardial Ischemia-Reperfusion Injury.

作者信息

Zu Lingyun, Wen Ningxin, Liu Changjie, Zhao Mingming, Zheng Lemin

机构信息

The Department of Cardiology, Peking University Third Hospital, Beijing 100191, China; Institute of Cardiovaslular Sciences, Peking University Health Science Center, Beijing 100191, China.

出版信息

Cardiovasc Hematol Disord Drug Targets. 2018;18(1):14-16. doi: 10.2174/1871529X16666161227143644.

DOI:10.2174/1871529X16666161227143644
PMID:28029075
Abstract

BACKGROUND

Recently, the treatment and prevention of ischemic cardiomyopathy is one of the emerging research topics in the cardiovascular field. Gap junction is the basic structure of cardiac electrophysiology. Connexin is the basic unit of gap junctions. Connexin43(CX43) is the most abundant member of Cx family in the heart, the normal expression of Cx43 is important for heart development, electrically coupled cardiomyocytes activities and coordination of myocardial function. The connection between Cx43 and myocardial ischemia/reperfusion or reperfusion injury has become the focus of current research.

METHODS

We undertook a structured search of bibliographic database for peer-reviewed research literature using a focused review question and inclusion/exclusion criteria. The quality of retrieved papers was appraised using standard tools. The characteristics of screened papers were described, and a deductive qualitative content analysis methodology was applied to analyze the interventions and findings of included studies using a conceptual framework.

RESULTS

Twenty-one papers were included in the review, eight papers outlined the relationship of Cx43 and reperfusion arrhythmias. Eight papers pointed out the effect on the infarct size of Cx43.

CONCLUSION

The findings of this review confirm that Cx43 is the most abundant member of Cx family in the heart and is vital for myocardial protection during ischemia/reperfusion process and for ischemia/reperfusion injury. Many of its mechanism are still not very clear and require future research in the future.

摘要

背景

近年来,缺血性心肌病的治疗与预防是心血管领域新兴的研究课题之一。缝隙连接是心脏电生理学的基本结构。连接蛋白是缝隙连接的基本单位。连接蛋白43(CX43)是心脏中连接蛋白家族中含量最丰富的成员,CX43的正常表达对心脏发育、心肌细胞电偶联活动及心肌功能协调至关重要。CX43与心肌缺血/再灌注或再灌注损伤之间的联系已成为当前研究的焦点。

方法

我们使用聚焦的综述问题和纳入/排除标准,对文献数据库进行结构化检索以获取同行评审的研究文献。使用标准工具评估检索到的论文质量。描述筛选论文的特征,并应用演绎性定性内容分析方法,使用概念框架分析纳入研究的干预措施和结果。

结果

本综述纳入21篇论文,其中8篇概述了CX43与再灌注心律失常的关系。8篇指出了CX43对梗死面积的影响。

结论

本综述结果证实,CX43是心脏中连接蛋白家族中含量最丰富的成员,对缺血/再灌注过程中的心肌保护及缺血/再灌注损伤至关重要。其许多机制仍不太清楚,有待未来进一步研究。

相似文献

1
Connexin43 and Myocardial Ischemia-Reperfusion Injury.连接蛋白43与心肌缺血-再灌注损伤
Cardiovasc Hematol Disord Drug Targets. 2018;18(1):14-16. doi: 10.2174/1871529X16666161227143644.
2
Effects of a reduction in the number of gap junction channels or in their conductance on ischemia-reperfusion arrhythmias in isolated mouse hearts.减少缝隙连接通道的数量或其电导率对分离的小鼠心脏缺血再灌注心律失常的影响。
Am J Physiol Heart Circ Physiol. 2011 Dec;301(6):H2442-53. doi: 10.1152/ajpheart.00540.2011. Epub 2011 Sep 23.
3
Endothelial Cx40 limits myocardial ischaemia/reperfusion injury in mice.内皮细胞 Cx40 限制小鼠心肌缺血/再灌注损伤。
Cardiovasc Res. 2014 May 1;102(2):329-37. doi: 10.1093/cvr/cvu063. Epub 2014 Mar 17.
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Interacting Network of the Gap Junction (GJ) Protein Connexin43 (Cx43) is Modulated by Ischemia and Reperfusion in the Heart.缝隙连接(GJ)蛋白连接蛋白43(Cx43)的相互作用网络受心脏缺血和再灌注的调节。
Mol Cell Proteomics. 2015 Nov;14(11):3040-55. doi: 10.1074/mcp.M115.052894. Epub 2015 Aug 27.
5
Inhibition of MicroRNA-206 Ameliorates Ischemia-Reperfusion Arrhythmia in a Mouse Model by Targeting Connexin43.miR-206 通过靶向连接蛋白 43 抑制小鼠模型缺血再灌注心律失常。
J Cardiovasc Transl Res. 2020 Aug;13(4):584-592. doi: 10.1007/s12265-019-09940-y. Epub 2019 Dec 2.
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Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection.缝隙连接蛋白 43 在心脏保护中的规范和非规范作用。
Biomolecules. 2020 Aug 23;10(9):1225. doi: 10.3390/biom10091225.
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Connexin 43 and ischemic preconditioning.连接蛋白43与缺血预处理
Cardiovasc Res. 2004 May 1;62(2):335-44. doi: 10.1016/j.cardiores.2003.12.017.
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Mitochondrial connexin 43 in sex-dependent myocardial responses and estrogen-mediated cardiac protection following acute ischemia/reperfusion injury.线粒体连接蛋白 43 在急性缺血/再灌注损伤后性别依赖性心肌反应和雌激素介导的心脏保护中的作用。
Basic Res Cardiol. 2019 Nov 18;115(1):1. doi: 10.1007/s00395-019-0759-5.
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Preconditioning in the absence or presence of sustained ischemia modulates myocardial Cx43 protein levels and gap junction distribution.在存在或不存在持续性缺血的情况下进行预处理,可调节心肌Cx43蛋白水平和缝隙连接分布。
Can J Physiol Pharmacol. 2001 May;79(5):371-8.
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Ischaemia-induced autophagy leads to degradation of gap junction protein connexin43 in cardiomyocytes.缺血诱导的自噬导致心肌细胞中缝隙连接蛋白连接蛋白43的降解。
Biochem J. 2015 Apr 15;467(2):231-45. doi: 10.1042/BJ20141370.

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Cohesin: an emerging master regulator at the heart of cardiac development.黏连蛋白:心脏发育中心的新兴主控调节剂。
Mol Biol Cell. 2023 May 1;34(5):rs2. doi: 10.1091/mbc.E22-12-0557. Epub 2023 Mar 22.
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Aquaporin 4 inhibition alleviates myocardial ischemia-reperfusion injury by restraining cardiomyocyte pyroptosis.水通道蛋白 4 抑制通过抑制心肌细胞焦亡减轻心肌缺血再灌注损伤。
Bioengineered. 2021 Dec;12(1):9021-9030. doi: 10.1080/21655979.2021.1992332.
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J Cardiovasc Dev Dis. 2021 May 5;8(5):52. doi: 10.3390/jcdd8050052.
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