Electrophysiological Mechanisms and Therapeutic Potential of Calcium Channels in Atrial Fibrillation

被引：0

作者：

Huang, Zuyuan ^{[1
]}

Luo, Cheng ^{[1
]}

Wu, Zimin ^{[1
]}

Zheng, Baoshi ^{[1
]}

机构：

[1] Guangxi Med Univ, Affiliated Hosp 1, Dept Cardiovasc Surg, Nanning 530021, Guangxi, Peoples R China

来源：

REVIEWS IN CARDIOVASCULAR MEDICINE | 2025年 / 26卷 / 06期

基金：

中国国家自然科学基金;

关键词：

atrial fibrillation; calcium channels; calcium homeostasis; electrophysiology; therapeutic targets; RYANODINE RECEPTOR FUNCTION; INDUCED CARDIAC FIBROSIS; DEPENDENT CA2+ RELEASE; HEART-FAILURE; DOWN-REGULATION; KINASE-II; INHIBITION; CAMKII; TRPM7; CRAC;

D O I：

10.31083/RCM33507

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Atrial fibrillation (AF) is a prevalent and complex arrhythmia for which the pathogenesis involves various electrophysiological factors, notably the regulation of calcium channels. This article aimed to investigate the specific roles and molecular mechanisms of the L-type and T-type calcium channels, ryanodine receptors (RyRs), inositol 1,4,5-triphosphate receptors (IP3Rs), calcium release-activated calcium (CRAC) channels, and transient receptor potential (TRP) channels in the pathogenesis and persistence of AF. In addition, this article reviews recent advances in calcium channel-targeted drugs from experimental and clinical studies, offering new insights into the relationship between calcium channel regulation and AF pathology. These findings suggest promising directions for further research into the mechanisms of AF and the development of targeted therapeutic strategies.

引用

页数：17

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