CircUBXN7 Impedes Apoptosis to Alleviate Myocardial Infarction Injury by Regulating the miR-582-3p/MARK3 Axis.

OBJECTIVE

The role of CircUBXN7 has been described in various disorders, including hypoxia/reoxygenation-induced cardiomyocyte injury. However, the detailed mechanisms underlying myocardial infarction (MI) remain unclear.

METHODS

CircUBXN7, microtubule affinity regulating kinase 3 (MARK3), and miR-582-3p expression was analyzed in patients with MI, in an ischemia/reperfusion (I/R) rat model, and in hypoxia-induced H9c2 cells using quantitative reverse transcription polymerase chain reaction analysis. The myocardial infarction (MI) area was assessed using triphenyltetrazolium chloride staining, whereas the TUNEL assay and western blotting were performed to assess apoptosis. The relationships of miR-582-3p with circUBXN7 and MARK3 3'UTR were ascertained through luciferase reporter experiments.

RESULTS

Both circUBXN7 and MARK3 were poorly expressed, whereas miR-582-3p was upregulated in patients with MI, the I/R rat model, and hypoxia-induced H9c2 cells. CircUBXN7 overexpression hampered hypoxia-induced apoptosis in H9c2 cells and mitigated MI-resulting myocardial injury. CircUBXN7 targeted miR-582-3p, and circUBXN7 overexpression abolished the pro-apoptotic influence of miR-582-3p overexpression in hypoxia-induced H9c2 cells. Nevertheless, the circUBXN7 target, MARK3, could abrogate the effect of the miR-582-3p mimic.

CONCLUSION

CircUBXN7 impedes apoptosis and reduces MI injury by regulating the miR-582-3p/MARK3 axis.