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<p>Cardiac injury resulting from exposure to fine particulate matter with aerodynamic diameter ≤2.5 μm (PM<sub>2.5</sub>) has been observed. Circular RNAs (circRNAs) play diverse roles in cardiac pathophysiology. Circ-ZNF609 has been reported to play important roles in doxorubicin-induced cardiotoxicity and myocardial ischemia-reperfusion injury. However, its role in PM<sub>2.5</sub>-induced myocardial injury remains unknown. In our research, we reported that down-regulation of circ-ZNF609 significantly reduced PM<sub>2.5</sub>-induced cardiomyocytes apoptosis as evidenced by decreased TUNEL positive cardiomyocytes, Bax/Bcl-2, and cleaved caspase-3/caspase-3 ratio, and increased cell viability as determined by CCK8. Interestingly, down-regulation of circ-ZNF609 inhibited the expression of YTHDF3. Moreover, YTHDF3 knockdown can rescue the aggravating effects of circ-ZNF609 overexpression on PM<sub>2.5</sub>-induced cardiomyocytes injury via reducing cardiomyocytes apoptosis and promoting cell viability. Circ-ZNF609 knockdown may alleviate PM<sub>2.5</sub>-induced cardiomyocyte injury, at least partially, by regulating YTHDF3 expression and mRNA stability. These findings provide preliminary evidence supporting the involvement of circ-ZNF609 in PM<sub>2.5</sub>-induced cardiomyocyte injury and warrant further investigation <i>in vivo</i>.</p>

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Downregulation of Circ-ZNF609 Reduces PM2.5-Induced Cardiomyocyte Injury Associated with Reduced YTHDF3 Expression

  • 期刊论文

  • 发表日期：

    2026年6月26日

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  • Yunwei Xu,
  • Junwen Tang,
  • Wenqin Zhou,
  • Wensi Wan,
  • Emeli Chatterjee,
  • Guoping Li,
  • Dragos Cretoiu,
  • Jiaqi Wang,
  • Lijun Wang

摘要

Cardiac injury resulting from exposure to fine particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5) has been observed. Circular RNAs (circRNAs) play diverse roles in cardiac pathophysiology. Circ-ZNF609 has been reported to play important roles in doxorubicin-induced cardiotoxicity and myocardial ischemia-reperfusion injury. However, its role in PM2.5-induced myocardial injury remains unknown. In our research, we reported that down-regulation of circ-ZNF609 significantly reduced PM2.5-induced cardiomyocytes apoptosis as evidenced by decreased TUNEL positive cardiomyocytes, Bax/Bcl-2, and cleaved caspase-3/caspase-3 ratio, and increased cell viability as determined by CCK8. Interestingly, down-regulation of circ-ZNF609 inhibited the expression of YTHDF3. Moreover, YTHDF3 knockdown can rescue the aggravating effects of circ-ZNF609 overexpression on PM2.5-induced cardiomyocytes injury via reducing cardiomyocytes apoptosis and promoting cell viability. Circ-ZNF609 knockdown may alleviate PM2.5-induced cardiomyocyte injury, at least partially, by regulating YTHDF3 expression and mRNA stability. These findings provide preliminary evidence supporting the involvement of circ-ZNF609 in PM2.5-induced cardiomyocyte injury and warrant further investigation in vivo.