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Background <p>Sepsis-induced myocardial injury (SIMI) commonly occurs as a complication of severe sepsis and septic shock. This research aims to explore the function of miR-222-3p inhibition in SIMI and its possible regulatory mechanisms.</p> Methods <p>A rat SIMI model was established using the cecal ligation and puncture method. In vitro experiments were conducted using lipopolysaccharide (LPS) to induce myocardial injury in H9C2 cells. miR-222-3p and MEGF9 expression were determined using qRT-PCR. Myocardial injury, inflammatory response, and oxidative stress indicators were detected using the ELISA and biochemical colorimetric assays. Cell viability and apoptosis were assessed using the CCK-8 method and flow cytometry. The interaction between miR-222-3p and MEGF9 was verified through a luciferase reporter gene assay.</p> Results <p>In the serum of rats with sepsis and LPS-induced H9C2 cells, miR-222-3p exhibited high expression, while MEGF9 was lowly expressed. Inhibition of miR-222-3p alleviated myocardial injury, inflammatory response, and oxidative stress in sepsis rats and LPS-induced cells, as evidenced by reduced CK-MB, cTnI, LDH, IL-6, IL-1β, TNF-α, and MDA level, and enhanced SOD activity. Inhibition of miR-222-3p increased LPS-induced cell viability and diminished apoptosis. miR-222-3p targeted MEGF9. Inhibiting MEGF9 expression could reverse the protective role of miR-222-3p suppression on LPS-induced myocardial injury.</p> Conclusion <p>This study’s results indicate that miR-222-3p exacerbates SIMI reactions by targeting and inhibiting MEGF9 expression. It is possible that miR-222-3p functions as a potential therapeutic target for SIMI.</p>

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miR-222-3p targeting MEGF9 exacerbates sepsis-induced myocardial injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月27日

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  • Weiwei Dou,
  • Zhenhua Wu,
  • Xue Yu,
  • Wei Wang,
  • Wei Chen

摘要

Background

Sepsis-induced myocardial injury (SIMI) commonly occurs as a complication of severe sepsis and septic shock. This research aims to explore the function of miR-222-3p inhibition in SIMI and its possible regulatory mechanisms.

Methods

A rat SIMI model was established using the cecal ligation and puncture method. In vitro experiments were conducted using lipopolysaccharide (LPS) to induce myocardial injury in H9C2 cells. miR-222-3p and MEGF9 expression were determined using qRT-PCR. Myocardial injury, inflammatory response, and oxidative stress indicators were detected using the ELISA and biochemical colorimetric assays. Cell viability and apoptosis were assessed using the CCK-8 method and flow cytometry. The interaction between miR-222-3p and MEGF9 was verified through a luciferase reporter gene assay.

Results

In the serum of rats with sepsis and LPS-induced H9C2 cells, miR-222-3p exhibited high expression, while MEGF9 was lowly expressed. Inhibition of miR-222-3p alleviated myocardial injury, inflammatory response, and oxidative stress in sepsis rats and LPS-induced cells, as evidenced by reduced CK-MB, cTnI, LDH, IL-6, IL-1β, TNF-α, and MDA level, and enhanced SOD activity. Inhibition of miR-222-3p increased LPS-induced cell viability and diminished apoptosis. miR-222-3p targeted MEGF9. Inhibiting MEGF9 expression could reverse the protective role of miR-222-3p suppression on LPS-induced myocardial injury.

Conclusion

This study’s results indicate that miR-222-3p exacerbates SIMI reactions by targeting and inhibiting MEGF9 expression. It is possible that miR-222-3p functions as a potential therapeutic target for SIMI.