Myocardial ischemia/reperfusion (I/R) injury is a common consequence of restored blood supply after acute myocardial infarction (AMI), but its underlying mechanisms remain largely elusive. In this study, we aimed to investigate the functional role of long non-coding RNA PVT1 in hypoxia/reoxygenation (H/R)-treated AC16 cardiomyocytes. Our experimental results demonstrated that H/R treatment impaired the viability and increased the apoptosis of AC16 cells, and knockdown of PVT1 blocked the H/R injury. Besides, PVT1 knockdown also reduced excessive autophagy in H/R-treated AC16 cells. Furthermore, we confirmed that PVT1 might serve as a ceRNA for miR-186 in AC16 cells, and rescue experiments showed that miR-186 inhibition blocked the effects of PVT1 knockdown in H/R-treated AC16 cells. In summary, this study implied that PVT1 might be a promising therapeutic target for treating myocardial I/R injury.

心肌缺血/再灌注（I / R）损伤是急性心肌梗塞（AMI）后恢复供血的常见结果，但其潜在机制仍很难捉摸。在这项研究中，我们旨在研究长的非编码RNA PVT1在缺氧/复氧（H / R）处理的AC16心肌细胞中的功能作用。我们的实验结果表明，H / R处理可损害AC16细胞的活力并增加其凋亡，而敲除PVT1则可阻止H / R损伤。此外，PVT1敲低还减少了经H / R处理的AC16细胞的过度自噬。此外，我们证实PVT1可能充当AC16细胞中miR-186的ceRNA，救援实验表明miR-186抑制作用抑制了经H / R处理的AC16细胞中PVT1敲低的作用。综上所述，