PUBLICATION
Particulate matter induces arrhythmia-like cardiotoxicity in zebrafish embryos by altering the expression levels of cardiac development- and ion channel-related genes
- Authors
- Park, K.H., Choi, Y.J., Min, W.K., Lee, S.H., Kim, J., Jeong, S.H., Lee, J.H., Choi, B.M., Kim, S.
- ID
- ZDB-PUB-230709-34
- Date
- 2023
- Source
- Ecotoxicology and environmental safety 263: 115201115201 (Journal)
- Registered Authors
- Kim, Suhyun
- Keywords
- Arrhythmia, Heart, Heavy metal, Ion channel, Particulate matter, Zebrafish
- MeSH Terms
-
- Animals
- Arrhythmias, Cardiac/chemically induced
- Arrhythmias, Cardiac/genetics
- Arrhythmias, Cardiac/metabolism
- Cardiotoxicity*/genetics
- Cardiotoxicity*/metabolism
- Embryo, Nonmammalian/metabolism
- Heart
- Ion Channels/genetics
- Particulate Matter/metabolism
- Particulate Matter/toxicity
- Zebrafish*/metabolism
- PubMed
- 37418944 Full text @ Ecotoxicol. Environ. Saf.
Citation
Park, K.H., Choi, Y.J., Min, W.K., Lee, S.H., Kim, J., Jeong, S.H., Lee, J.H., Choi, B.M., Kim, S. (2023) Particulate matter induces arrhythmia-like cardiotoxicity in zebrafish embryos by altering the expression levels of cardiac development- and ion channel-related genes. Ecotoxicology and environmental safety. 263:115201115201.
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping