This study aimed to explore the molecular mechanism of myocardial protection. The effects of miR-32-3p and ring finger protein 13 (RNF13) on endoplasmic reticulum (ER) stress-induced apoptosis of A-10 cells and human umbilical vein endothelial cells (HUVEC) were detected using flow cytometry. The effects of miR-32-3p and phenylbutyric acid (PBA) on plaque instability and myocardial tissue injury in rats were investigated after establishment of arterial plaque model and embolization model and treatment with miR-32-3p-antagomir and PBA. RNF13, which was differentially expressed in myocardial infarction, was the direct target gene of miR-32-3p. MiR-32-3p inhibited RNF13 expression and targeted RNF13 to inhibit ER stress-induced cell apoptosis. Furthermore, inhibiting miR-32-3p expression induced arterial plaque instability by reducing survival, increasing pathological lesions in arterial tissue, up-regulating ER stress-related proteins, and regulating the expressions of apoptosis-related proteins in the model rats. However, PBA reversed the effects of miR-32-3p-antagomir on the model rats.

Graphical abstract

中文翻译：

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MiR-32-3p 通过靶向 RNF13 调节微栓塞和微血管阻塞引起的心肌损伤以调节动脉粥样硬化斑块的稳定性

本研究旨在探讨心肌保护的分子机制。流式细胞仪检测miR-32-3p和无名指蛋白13（RNF13）对内质网（ER）应激诱导的A-10细胞和人脐静脉内皮细胞（HUVEC）凋亡的影响。在建立动脉斑块模型和栓塞模型并用miR-32-3p-antagomir和PBA治疗后，研究了miR-32-3p和苯基丁酸（PBA）对大鼠斑块不稳定性和心肌组织损伤的影响。RNF13在心肌梗死中差异表达，是miR-32-3p的直接靶基因。MiR-32-3p 抑制 RNF13 表达并靶向 RNF13 以抑制 ER 应激诱导的细胞凋亡。此外，抑制 miR-32-3p 表达会通过降低存活率来诱导动脉斑块不稳定性，增加模型大鼠动脉组织病理病变，上调内质网应激相关蛋白，调节凋亡相关蛋白的表达。然而，PBA 逆转了 miR-32-3p-antagomir 对模型大鼠的影响。

图形概要