Upregulation of miR-143-3p attenuates oxidative stress-mediated cell ferroptosis in cardiomyocytes with atrial fibrillation by degrading glutamic-oxaloacetic transaminase 1

Oxidative stress-mediated cell death in cardiomyocytes contributes to the development of atrial fibrillation.However,the detailed mechanisms are still unclear.In the present study,we established atrial fibrillation models in mice.The cardiomyocytes were isolated from atrial fibrillation mice and normal mice and were cultured in vitro,respectively.The results showed that cell proliferation and viability in cardiomyocytes with atrial fibrillation were significantly lower than the cells from the normal mice.Consistently,atrial fibrillation cardiomyocytes were prone to suffer from apoptotic cell death.Also,the oxidative stress and ferroptosis-associated signatures were significantly increased in atrial fibrillation cardiomyocytes compared to normal cardiomyocytes,and ferroptosis inhibitor and NAC rescued cell viability in atrial fibrillation cardiomyocytes during in vitro cell culture.In addition,low-expressed miR-143-3p was observed in atrial fibrillation cardiomyocytes compared to normal cardiomyocytes,and overexpression of miR-143-3p increased cell proliferation and inhibited cell death in atrial fibrillation cardiomyocytes.Furthermore,glutamic-oxaloacetic transaminase 1 could be negatively regulated by miR-143-3p in normal cardiomyocytes,and miR-143-3p overexpression inhibited cell ferroptosis in atrial fibrillation cardiomyocytes by sponging glutamic-oxaloacetic transaminase 1.Collectively,overexpression of miR-143-3p increased cell viability and promoted cell proliferation in cardiomyocytes with atrial fibrillation by inhibiting glutamic-oxaloacetic transaminase 1 mediated oxidative damages and cell ferroptosis.