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Background <p>Circular RNAs (circRNAs) are believed to play a role in various human diseases, but their involvement in acute myocardial infarction (AMI) remains poorly understood. This study aims to clarify the role of hsa_circ_0081241 in AMI and elucidate its mechanism of action.</p> Methods <p>RT-qPCR and western blotting detected the expression of hsa_circ_0081241, miR-15b-5p, and PHD finger protein 19 (PHF19). A dual-luciferase reporter assay demonstrated their targeting relationships. Cell viability and apoptosis were assessed using CCK-8 and Annexin V-FITC/PI kits. M1 polarization of human bone marrow macrophages (hBMMs) was evaluated by detecting iNOS and CD68/CD86 expression. ELISA kits measured IL-6 and IL-12 secretion levels. Collagen I/III expression was measured to assess fibrosis. Reactive oxygen species (ROS) and superoxide dismutase (SOD) levels were measured to evaluate oxidative stress damage. The clinical value of the hsa_circ_0081241/miR-15b-5p/PHF19 axis was assessed using receiver operating characteristic (ROC) curves and a binary logistic regression model.</p> Results <p>Hsa_circ_0081241 promoted hypoxia-induced functional impairment in human cardiomyocytes (AC16) and mediated M1 polarization of hBMMs, driving fibrosis progression in human myocardial fibroblasts (hMFs). Pro-inflammatory factors secreted by M1 macrophages further aggravated hMF fibrosis. Hsa_circ_0081241 promoted PHF19 expression by down-regulating miR-15b-5p, mediating oxidative stress injury in hypoxia/reoxygenation (H/R)-damaged AC16 cells and myocardial tissues of the AMI rat model. Hsa_circ_0081241, miR-15b-5p, and PHF19 were independent predictors of AMI, with a combined area under the curve (AUC) of 0.871.</p> Conclusion <p>The hsa_circ_0081241/miR-15b-5p/PHF19 signaling axis is a potential biomarker for AMI. It may play an important role in myocardial injury caused by hypoxia and inflammatory microenvironments in this disease context.</p>

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Hsa_circ_0081241 is involved in the progression of acute myocardial infarction through the miR-15b-5p/PHF19 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月17日

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  • Lei Zhou,
  • Xiaochun Feng,
  • Kun Zhang,
  • Wei Song,
  • Bing Liu,
  • Shun Xiao,
  • Mingjin Guo,
  • Zhengnan Zhang

摘要

Background

Circular RNAs (circRNAs) are believed to play a role in various human diseases, but their involvement in acute myocardial infarction (AMI) remains poorly understood. This study aims to clarify the role of hsa_circ_0081241 in AMI and elucidate its mechanism of action.

Methods

RT-qPCR and western blotting detected the expression of hsa_circ_0081241, miR-15b-5p, and PHD finger protein 19 (PHF19). A dual-luciferase reporter assay demonstrated their targeting relationships. Cell viability and apoptosis were assessed using CCK-8 and Annexin V-FITC/PI kits. M1 polarization of human bone marrow macrophages (hBMMs) was evaluated by detecting iNOS and CD68/CD86 expression. ELISA kits measured IL-6 and IL-12 secretion levels. Collagen I/III expression was measured to assess fibrosis. Reactive oxygen species (ROS) and superoxide dismutase (SOD) levels were measured to evaluate oxidative stress damage. The clinical value of the hsa_circ_0081241/miR-15b-5p/PHF19 axis was assessed using receiver operating characteristic (ROC) curves and a binary logistic regression model.

Results

Hsa_circ_0081241 promoted hypoxia-induced functional impairment in human cardiomyocytes (AC16) and mediated M1 polarization of hBMMs, driving fibrosis progression in human myocardial fibroblasts (hMFs). Pro-inflammatory factors secreted by M1 macrophages further aggravated hMF fibrosis. Hsa_circ_0081241 promoted PHF19 expression by down-regulating miR-15b-5p, mediating oxidative stress injury in hypoxia/reoxygenation (H/R)-damaged AC16 cells and myocardial tissues of the AMI rat model. Hsa_circ_0081241, miR-15b-5p, and PHF19 were independent predictors of AMI, with a combined area under the curve (AUC) of 0.871.

Conclusion

The hsa_circ_0081241/miR-15b-5p/PHF19 signaling axis is a potential biomarker for AMI. It may play an important role in myocardial injury caused by hypoxia and inflammatory microenvironments in this disease context.