Myocardial infarction (MI) leads to cardiac remodelling and heart failure. Cardiomyocyte apoptosis is considered a critical pathological phenomenon accompanying MI, but the pathogenesis mechanism remains to be explored. MicroRNAs (miRs), with the identity of negative regulator of gene expression, exist as an important contributor to apoptosis. During the experiment of this study, MI mice models were successfully established and sequencing data showed that the expression of miR‐23a‐5p was significantly enhanced during MI progression. Further steps were taken and it showed that apoptosis of cardiac cells weakened as miR‐23a‐5p was downregulated and on the contrary that apoptosis strengthened with the overexpression of miR‐23a‐5p. To explore its working mechanisms, bioinformatics analysis was conducted by referring to multi‐databases to predict the targets of miR‐23a‐5p. Further analysis suggested that those downstream genes enriched in several pathways, especially in the PI3K/Akt singling pathway. Furthermore, it demonstrated that miR‐23a‐5p was negatively related to the phosphorylation of PI3K/Akt, which plays a critical role in triggering cell apoptosis during MI. Recilisib‐activated PI3K/Akt singling pathway could restrain apoptosis from inducing miR‐23a‐5p overexpression, and Miltefosine‐blocked PI3K/Akt singling pathway could restrict apoptosis from inhibiting miR‐23a‐5p reduction. In conclusion, these findings revealed the pivotal role of miR‐23a‐5p‐PI3K/Akt axis in regulating apoptosis during MI, introducing this novel axis as a potential indicator to detect ischemic heart disease and it could be used for therapeutic intervention.

中文翻译：

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microRNA-23a-5p的过表达通过抑制PI3K / AKT信号通路来促进心肌细胞凋亡，从而诱发心肌梗塞。

心肌梗塞（MI）会导致心脏重塑和心力衰竭。心肌细胞凋亡被认为是伴随MI的关键病理现象，但其发病机理仍有待探索。MicroRNA（miRs）具有基因表达的负调控因子，是导致细胞凋亡的重要因素。在这项研究的实验过程中，成功建立了MI小鼠模型，测序数据显示miR-23a-5p的表达在MI进展过程中显着增强。采取了进一步的措施，结果表明，随着miR-23a-5p的下调，心肌细胞的凋亡减弱，相反，随着miR-23a-5p的过表达，凋亡增强。为了探索其工作机制，通过参考多个数据库进行生物信息学分析，以预测miR-23a-5p的目标。进一步的分析表明，那些下游基因富集了几种途径，尤其是在PI3K / Akt单一途径中。此外，它表明miR-23a-5p与PI3K / Akt的磷酸化负相关，这在MI期间触发细胞凋亡中起着关键作用。Recilisib激活的PI3K / Akt单一通路可能抑制凋亡诱导miR-23a-5p过表达，而Miltefosine阻断的PI3K / Akt单一通路可能抑制凋亡抑制miR-23a-5p降低。总之，这些发现揭示了miR-23a-5p-PI3K / Akt轴在MI期间调控细胞凋亡中的关键作用，