Suppr超能文献

药物治疗病态窦房结综合征。

Pharmacologic Approach to Sinoatrial Node Dysfunction.

机构信息

Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, 34096 Montpellier, France; email:

LabEx Ion Channels Science and Therapeutics (ICST), 06560 Nice, France.

出版信息

Annu Rev Pharmacol Toxicol. 2021 Jan 6;61:757-778. doi: 10.1146/annurev-pharmtox-031120-115815. Epub 2020 Oct 5.

Abstract

The spontaneous activity of the sinoatrial node initiates the heartbeat. Sino-atrial node dysfunction (SND) and sick sinoatrial (sick sinus) syndrome are caused by the heart's inability to generate a normal sinoatrial node action potential. In clinical practice, SND is generally considered an age-related pathology, secondary to degenerative fibrosis of the heart pacemaker tissue. However, other forms of SND exist, including idiopathic primary SND, which is genetic, and forms that are secondary to cardiovascular or systemic disease. The incidence of SND in the general population is expected to increase over the next half century, boosting the need to implant electronic pacemakers. During the last two decades, our knowledge of sino-atrial node physiology and of the pathophysiological mechanisms underlying SND has advanced considerably. This review summarizes the current knowledge about SND mechanisms and discusses the possibility of introducing new pharmacologic therapies for treating SND.

摘要

窦房结的自发性活动启动心跳。窦房结功能障碍(SND)和病态窦房结(病态窦房结)综合征是由于心脏无法产生正常的窦房结动作电位引起的。在临床实践中,SND 通常被认为是一种与年龄相关的病理学,继发于心脏起搏器组织的退行性纤维化。然而,其他形式的 SND 也存在,包括原发性 SND,这是遗传性的,以及继发于心血管或系统性疾病的形式。预计在未来半个世纪,SND 在普通人群中的发病率将会增加,这将增加对植入电子起搏器的需求。在过去的二十年中,我们对窦房结生理学和 SND 病理生理机制的认识有了很大的提高。这篇综述总结了目前关于 SND 机制的知识,并讨论了引入新的药物治疗 SND 的可能性。

相似文献

1
Pharmacologic Approach to Sinoatrial Node Dysfunction.
Annu Rev Pharmacol Toxicol. 2021 Jan 6;61:757-778. doi: 10.1146/annurev-pharmtox-031120-115815. Epub 2020 Oct 5.
2
Sinus node dysfunction: current understanding and future directions.
Am J Physiol Heart Circ Physiol. 2023 Mar 1;324(3):H259-H278. doi: 10.1152/ajpheart.00618.2022. Epub 2022 Dec 23.
3
Emerging Signaling Regulation of Sinoatrial Node Dysfunction.
Curr Cardiol Rep. 2023 Jul;25(7):621-630. doi: 10.1007/s11886-023-01885-8. Epub 2023 May 25.
5
Sick sinus syndrome in HCN1-deficient mice.
Circulation. 2013 Dec 17;128(24):2585-94. doi: 10.1161/CIRCULATIONAHA.113.003712. Epub 2013 Nov 11.
6
Genetic Complexity of Sinoatrial Node Dysfunction.
Front Genet. 2021 Apr 1;12:654925. doi: 10.3389/fgene.2021.654925. eCollection 2021.
7
Relationship between two arrhythmias: sinus node dysfunction and atrial fibrillation.
Arch Med Res. 2014 May;45(4):351-5. doi: 10.1016/j.arcmed.2014.04.005. Epub 2014 May 11.
8
Molecular Signatures of Sinus Node Dysfunction Induce Structural Remodeling in the Right Atrial Tissue.
Mol Cells. 2020 Apr 30;43(4):408-418. doi: 10.14348/molcells.2020.2164.
10
TBX18 overexpression enhances pacemaker function in a rat subsidiary atrial pacemaker model of sick sinus syndrome.
J Physiol. 2018 Dec;596(24):6141-6155. doi: 10.1113/JP276508. Epub 2018 Oct 13.

引用本文的文献

1
Role of Cav1.3 Channels in Brain-Heart Interactions: An Unexpected Journey.
Biomedicines. 2025 Jun 4;13(6):1376. doi: 10.3390/biomedicines13061376.
2
Aging and sinus node dysfunction: mechanisms and future directions.
Clin Sci (Lond). 2025 Jun 11;139(11):577-93. doi: 10.1042/CS20231025.
3
Causality of Childhood and Adult Body Mass Index on Sick Sinus Syndrome: A Mendelian Randomization Study.
Cureus. 2025 Mar 20;17(3):e80913. doi: 10.7759/cureus.80913. eCollection 2025 Mar.
4
Opto-chemogenetic inhibition of L-type Ca1 channels in neurons through a membrane-assisted molecular linkage.
Cell Rep Methods. 2024 Nov 18;4(11):100898. doi: 10.1016/j.crmeth.2024.100898. Epub 2024 Nov 7.
5
Pathophysiology, molecular mechanisms, and genetics of atrial fibrillation.
Hum Cell. 2024 Nov 6;38(1):14. doi: 10.1007/s13577-024-01145-z.
6
Pacemaker Channels and the Chronotropic Response in Health and Disease.
Circ Res. 2024 May 10;134(10):1348-1378. doi: 10.1161/CIRCRESAHA.123.323250. Epub 2024 May 9.
8
Ivabradine could not decrease mitral regurgitation triggered atrial fibrosis and fibrillation compared with carvedilol.
ESC Heart Fail. 2024 Feb;11(1):251-260. doi: 10.1002/ehf2.14577. Epub 2023 Nov 14.
9
Lipopolysaccharide-induced sepsis impairs M2R-GIRK signaling in the mouse sinoatrial node.
Proc Natl Acad Sci U S A. 2023 Jul 11;120(28):e2210152120. doi: 10.1073/pnas.2210152120. Epub 2023 Jul 5.
10
Emerging Signaling Regulation of Sinoatrial Node Dysfunction.
Curr Cardiol Rep. 2023 Jul;25(7):621-630. doi: 10.1007/s11886-023-01885-8. Epub 2023 May 25.

本文引用的文献

4
Cardiac Pacemaker Activity and Aging.
Annu Rev Physiol. 2020 Feb 10;82:21-43. doi: 10.1146/annurev-physiol-021119-034453. Epub 2019 Nov 22.
6
Functional Characterization of Rare Variants in the Gene Identified in Sinus Node Dysfunction and Atrial Fibrillation.
Front Genet. 2019 Jul 11;10:648. doi: 10.3389/fgene.2019.00648. eCollection 2019.
8
Efficacy of cilostazol for sick sinus syndrome to avoid permanent pacemaker implantation: A retrospective case-control study.
J Cardiol. 2019 Oct;74(4):328-332. doi: 10.1016/j.jjcc.2019.03.007. Epub 2019 Apr 11.
9
Mutant KCNJ3 and KCNJ5 Potassium Channels as Novel Molecular Targets in Bradyarrhythmias and Atrial Fibrillation.
Circulation. 2019 Apr 30;139(18):2157-2169. doi: 10.1161/CIRCULATIONAHA.118.036761.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验