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颗粒物通过改变心脏发育和离子通道相关基因的表达水平诱导斑马鱼胚胎发生心律失常样心脏毒性。

Particulate matter induces arrhythmia-like cardiotoxicity in zebrafish embryos by altering the expression levels of cardiac development- and ion channel-related genes.

机构信息

Department of Pediatrics, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.

Department of Anesthesiology and Pain Medicine, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.

出版信息

Ecotoxicol Environ Saf. 2023 Sep 15;263:115201. doi: 10.1016/j.ecoenv.2023.115201. Epub 2023 Jul 5.

Abstract

Air pollution is a risk factor that increases cardiovascular morbidity and mortality. In this study, we investigated the cardiotoxicity of particulate matter (PM) exposure using a zebrafish embryo model. We found that PM exposure induced cardiotoxicity, such as arrhythmia, during cardiac development. PM exposure caused cardiotoxicity by altering the expression levels of cardiac development (T-box transcription factor 20, natriuretic peptide A, and GATA-binding protein 4)- and ion-channel (scn5lab, kcnq1, kcnh2a/b, and kcnh6a/b)-related genes. In conclusion, this study showed that PM induces the aberrant expression of cardiac development- and ion channel-related genes, leading to arrhythmia-like cardiotoxicity in zebrafish embryos. Our study provides a foundation for further research on the molecular and genetic mechanisms of cardiotoxicity induced by PM exposure.

摘要

空气污染是增加心血管发病率和死亡率的风险因素。在这项研究中,我们使用斑马鱼胚胎模型研究了颗粒物(PM)暴露的心脏毒性。我们发现 PM 暴露在心脏发育过程中会引起心脏毒性,如心律失常。PM 暴露通过改变心脏发育(T 盒转录因子 20、利钠肽 A 和 GATA 结合蛋白 4)和离子通道(scn5lab、kcnq1、kcnh2a/b 和 kcnh6a/b)相关基因的表达水平引起心脏毒性。总之,这项研究表明,PM 诱导心脏发育和离子通道相关基因的异常表达,导致斑马鱼胚胎出现类似心律失常的心脏毒性。我们的研究为进一步研究 PM 暴露引起的心脏毒性的分子和遗传机制提供了基础。

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