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<p>Myocardial infarction (MI) is a leading cause of death and disability worldwide. The promotion of myocardial regeneration is a promising therapeutic strategy for acute MI. Using a zebrafish ventricular ablation system, we found that the Mongolian traditional medicine Eerdun-Wurile (EW) promotes myocardial regeneration in zebrafish. EW treatment significantly accelerated proliferation of myocardial cells and improved cardiac function. Transcriptome sequencing revealed a significant decrease in mevalonate diphosphate decarboxylase a (<i>mvda</i>) expression in the metronidazole-induced ventricular ablation group, whereas <i>mvda</i> expression was restored in the EW group. <i>mvda</i> knockdown using morpholino oligonucleotides reversed the EW-mediated myocardial regeneration, whereas <i>mvda</i> overexpression enhanced the regenerative ability. In conclusion, EW may promote zebrafish myocardial regeneration, accelerate myocardial cell proliferation, and improve cardiac function by upregulating <i>mvda</i> expression. Our data partially revealed the molecular mechanism by which EW promotes myocardial regeneration and repair, and provides experimental data and novel insights for advancing MI treatment.</p>

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Mongolian medicine Eerdun-Wurile promotes myocardial regeneration by regulating MVDA in zebrafish

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月6日

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  • Xianghui Chen,
  • Xiaoting Li,
  • Jiajun Sun,
  • Yufeng Lin,
  • Yuanhao Li,
  • Xuehao Lv,
  • Rui Zhao,
  • Xinyue Gu,
  • Wenxuan Wang,
  • Yabin Xie,
  • Wei Xie,
  • Rengui Bade,
  • Shuyuan Jiang,
  • Xiaolei Liu,
  • Bo Zou,
  • Yannan Bi,
  • Guo Shao,
  • Haihua Bai,
  • Wei Zhu,
  • Xiaoe Jia

摘要

Myocardial infarction (MI) is a leading cause of death and disability worldwide. The promotion of myocardial regeneration is a promising therapeutic strategy for acute MI. Using a zebrafish ventricular ablation system, we found that the Mongolian traditional medicine Eerdun-Wurile (EW) promotes myocardial regeneration in zebrafish. EW treatment significantly accelerated proliferation of myocardial cells and improved cardiac function. Transcriptome sequencing revealed a significant decrease in mevalonate diphosphate decarboxylase a (mvda) expression in the metronidazole-induced ventricular ablation group, whereas mvda expression was restored in the EW group. mvda knockdown using morpholino oligonucleotides reversed the EW-mediated myocardial regeneration, whereas mvda overexpression enhanced the regenerative ability. In conclusion, EW may promote zebrafish myocardial regeneration, accelerate myocardial cell proliferation, and improve cardiac function by upregulating mvda expression. Our data partially revealed the molecular mechanism by which EW promotes myocardial regeneration and repair, and provides experimental data and novel insights for advancing MI treatment.