MicroRNAs (miRNAs) play various roles in the regulation of human disease, including cardiovascular diseases. MiR-153 has been previously shown to be involved in regulating neuron survival during cerebral ischemia/reperfusion (I/R) injury. However, whether miR-153 is involved in I/R-induced cardiomyocyte apoptosis remains to be elucidated. In this study, we aimed to explore the role of miR-153 in the regulation of I/R-induced cardiomyocyte apoptosis and to investigate the miR-153-mediated molecular signaling pathway responsible for its effect on cardiomyocytes using an oxygen-glucose deprivation and reoxygenation (OGD/R) cellular model. We found that OGD/R treatment induced significant upregulation of miR-153 in cardiomyocytes causing reactive oxygen species (ROS) production and cell apoptosis signaling activation and subsequently leading to cardiomyocyte apoptosis. Suppression of miR-153 protected cardiomyocytes against OGD/R treatment. We further identified that nuclear factor-like 2 (Nrf2) is a functional target of miR-153. Nrf2/ heme oxygenase-1 (HO-1) signaling plays a critical role in miR-153 regulated OGD/R-induced cardiomyocyte apoptosis. Our study indicates that the inhibition of miR-153 or restoration of Nrf2 may serve as a potential therapeutic strategy for ischemia/reperfusion injury prevention.

中文翻译：

---

MiR-153通过靶向Nrf2 / HO-1信号传导来调节心肌细胞凋亡。

微小RNA（miRNA）在调节人类疾病（包括心血管疾病）中扮演着各种角色。先前已证明，MiR-153参与调节脑缺血/再灌注（I / R）损伤期间的神经元存活。然而，miR-153是否参与I / R诱导的心肌细胞凋亡仍有待阐明。在这项研究中，我们旨在探讨miR-153在I / R诱导的心肌细胞凋亡调控中的作用，并研究利用氧-葡萄糖剥夺法和miR-153介导的分子信号通路对心肌细胞的影响。复氧（OGD / R）细胞模型。我们发现，OGD / R处理可引起心肌细胞中miR-153的显着上调，从而导致活性氧（ROS）产生和细胞凋亡信号传导激活，进而导致心肌细胞凋亡。抑制miR-153保护的心肌细胞不受OGD / R处理。我们进一步确定，核因子样2（Nrf2）是miR-153的功能目标。Nrf2 /血红素加氧酶-1（HO-1）信号传导在miR-153调节的OGD / R诱导的心肌细胞凋亡中起关键作用。我们的研究表明，抑制miR-153或恢复Nrf2可以作为预防缺血/再灌注损伤的潜在治疗策略。我们进一步确定，核因子样2（Nrf2）是miR-153的功能目标。Nrf2 /血红素加氧酶-1（HO-1）信号传导在miR-153调节的OGD / R诱导的心肌细胞凋亡中起关键作用。我们的研究表明，抑制miR-153或恢复Nrf2可能是预防缺血/再灌注损伤的潜在治疗策略。我们进一步确定，核因子样2（Nrf2）是miR-153的功能目标。Nrf2 /血红素加氧酶-1（HO-1）信号在miR-153调节的OGD / R诱导的心肌细胞凋亡中起关键作用。我们的研究表明，抑制miR-153或恢复Nrf2可能是预防缺血/再灌注损伤的潜在治疗策略。