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Particulate matter induces arrhythmia-like cardiotoxicity in zebrafish embryos by altering the expression levels of cardiac development- and ion channel-related genes.
Park, Kyu Hee; Choi, Yoon Ji; Min, Won Kee; Lee, Sun Hwa; Kim, Jaeyoung; Jeong, Sang Hoon; Lee, Ju-Han; Choi, Byung Min; Kim, Suhyun.
Afiliação
  • Park KH; Department of Pediatrics, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.
  • Choi YJ; Department of Anesthesiology and Pain Medicine, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.
  • Min WK; Department of Anesthesiology and Pain Medicine, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.
  • Lee SH; Zebrafish Translational Medical Research Center, Korea University, Ansan 15588, Gyeonggi-do, the Republic of Korea.
  • Kim J; Medical Science Research Center, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.
  • Jeong SH; Medical Science Research Center, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.
  • Lee JH; Department of Pathology, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.
  • Choi BM; Department of Pediatrics, Ansan Hospital, Korea University College of Medicine, Ansan 15588, the Republic of Korea.
  • Kim S; Department of Biomedical Sciences, College of Medicine, Korea University, Seoul 04763, the Republic of Korea; Zebrafish Translational Medical Research Center, Korea University, Ansan 15588, Gyeonggi-do, the Republic of Korea. Electronic address: dieslunae@korea.ac.kr.
Ecotoxicol Environ Saf ; 263: 115201, 2023 Sep 15.
Article em En | MEDLINE | ID: mdl-37418944
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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Peixe-Zebra / Cardiotoxicidade Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Peixe-Zebra / Cardiotoxicidade Idioma: En Ano de publicação: 2023 Tipo de documento: Article