Role of TRPM4 ion channel in pediatric arrhythmic syndromes.

World journal of clinical pediatrics Pub Date : 2026-06-09 DOI:10.5409/wjcp.v15.i2.114189

Olesya V Melnik, Olga E Kulichik, Anastasiya K Zaytseva, Olga A Kofeynikova, Svetlana G Fetisova, Svetlana I Tarnovskaya, Yuliya V Fomicheva, Elena S Vasichkina, Boris S Zhorov, Olga V Kalinina, Anna A Kostareva

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引用次数: 0

Abstract

TRPM4 is a member of transient receptor potential (TRP) ion channel group which greatly contributes to cardiomyocyte function and physiology. It controls the dynamic stabilization of calcium level and is involved in sinus node regulation and cardiac conduction. Most of pathogenic variants in TRPM4 gene are associated with conduction disorders and various types of arrhythmic syndromes presenting in children and early adolescents. In addition, TRPM4 gain- and loss-of-function variants are discussed in connection to Brugada syndrome and long QT-syndrome. In this review we summarize current knowledge on the role of TRPM4 variants in pediatric arrhythmic syndromes, discuss molecular mechanisms of TRPM4 dysfunction, provide clinical illustrations and case presentations underlining the role of TRPM4 in molecular pathogenesis of arrhythmic syndromes presented in young age.

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TRPM4离子通道在儿童心律失常综合征中的作用。

TRPM4是瞬时受体电位（TRP）离子通道群的成员，对心肌细胞的功能和生理有重要作用。它控制钙水平的动态稳定，并参与窦房结调节和心脏传导。TRPM4基因的大多数致病性变异与儿童和青少年早期出现的传导障碍和各种类型的心律失常综合征有关。此外，还讨论了TRPM4的功能增加和功能丧失变异与Brugada综合征和long qt综合征的关系。在这篇综述中，我们总结了目前关于TRPM4变异在儿童心律失常综合征中的作用的知识，讨论了TRPM4功能障碍的分子机制，提供了临床例证和病例报告，强调了TRPM4在幼年心律失常综合征分子发病机制中的作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

World journal of clinical pediatrics

CiteScore

3.20

自引率

0.00%

发文量