Circular RNA (circRNA) MFACR promotes cardiomyocyte death that leads to myocardial infarction (MI). This study aimed to explore the role of MFACR in MI.RT-qPCRs were performed to measure the expression levels of MFACR and miR-125b in plasma samples from both MI patients (n = 61) and healthy controls (n = 61). MFACR or miR-125b was overexpressed in AC16 cells (cardiomyocytes) to explore the interaction between them. Methylation of miR-125b gene in cells with the overexpression of MFACR was detected by methylation-specific PCR. Cell apoptosis after transfections was detected by cell apoptosis assay. MI model was constructed to further demonstrate the effect of MFACR in vivo.We found that MFACR was upregulated in MI and inversely correlated with miR-125b. In AC16 cells, hypoxia treatment increased the expression levels of MFACR and decreased the expression levels of miR-125b. In AC16 cells, overexpression of MFACR decreased the expression levels of miR-125b and increased the methylation of miR-125b gene. Under hypoxia treatment, overexpression of MFACR increased AC16 cell apoptosis, and overexpression of miR-125b decreased cell apoptosis. In addition, overexpression of miR-125b reversed the effects of overexpression of MFACR on cell apoptosis both in vivo and in vitro.MFACR may increase the methylation of miR-125b gene to downregulate its expression, thereby promoting the apoptosis of cardiomyocytes in MI.

中文翻译：

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CircRNA MFACR 在心肌梗塞中上调并下调 miR-125b 以促进缺氧诱导的心肌细胞凋亡。

环状 RNA (circRNA) MFACR 促进心肌细胞死亡，从而导致心肌梗死 (MI)。本研究旨在探讨 MFACR 在 MI 中的作用。采用 RT-qPCR 来测量 MI 患者 (n = 61) 和健康对照 (n = 61) 血浆样本中 MFACR 和 miR-125b 的表达水平。MFACR 或 miR-125b 在 AC16 细胞（心肌细胞）中过表达，以探索它们之间的相互作用。通过甲基化特异性PCR检测MFACR过表达细胞中miR-125b基因的甲基化。细胞凋亡实验检测转染后细胞凋亡情况。构建MI模型以进一步证明MFACR在体内的作用。我们发现MFACR在MI中表达上调，并且与miR-125b呈负相关。在AC16细胞中，缺氧处理增加了MFACR的表达水平并降低了miR-125b的表达水平。在AC16细胞中，MFACR的过度表达降低了miR-125b的表达水平并增加了miR-125b基因的甲基化。缺氧处理下，MFACR过表达会增加AC16细胞凋亡，而miR-125b过表达会减少细胞凋亡。此外，在体内和体外，miR-125b的过表达逆转了MFACR过表达对细胞凋亡的影响。MFACR可能增加miR-125b基因的甲基化，下调其表达，从而促进MI心肌细胞凋亡。