<scp>XIST</scp> Improves Mitophagy and Exerts Perioperative Myocardial Protection Through <scp>miR</scp> ‐212‐3p/ <scp>CALCOCO2</scp> / <scp>OPTN</scp>

Acute coronary syndrome (ACS) is a high-risk disease among cardiovascular diseases. This study is to screen for lncRNA ceRNA regulatory network in acute coronary syndrome associated with percutaneous coronary intervention (PCI) and to validate the XIST/miR-212-3p/CALCOCO2/OPTN axes. lncRNA, miRNA, and mRNA expression microarray data were retrieved and downloaded from the GEO database. Dysregulated lncRNAs and miRNAs were collected using the GEO database. Target genes were predicted and subjected to KEGG pathway analysis. The serum levels of lncRNA XIST, miR-212-3p, CALCOCO2, and OPTN were detected by RT-qPCR. The H9C2 hypoxia-reoxygenation (H/R) injury model was established. The cell viability was detected. The related indicators of mitophagy were detected by flow cytometry and Western blot. Six PCI-related lncRNAs were identified in ACS, linked to 44 PCI-associated miRNAs and 159 PCI-associated mRNAs. KEGG pathway analysis suggested the mitophagy pathway, which involved XIST/miR-212-3p/CALCOCO2/OPTN axes. The levels of XIST, CALCOCO2, and OPTN were increased while the level of miR-212-3p was decreased in PCI patients. Taken together, our results suggest that lncRNA-miRNA-mRNA networks associated with PCI in ACS were presented. In the H/R cell model, XIST promoted mitophagy through miR-212-3p/CALCOCO2/OPTN. XIST can promote mitophagy through the miR-212-3p/CALCOCO2/OPTN axis, thereby alleviating myocardial cell injury.