Myocardial infarction (MI) is one of the leadingcauses of high mortality worldwide. Long non-codingRNA myocardial infarction associated transcript (MIAT)and mitochondrial coupling factor 6 (CF6) aggravate MI. This study aimed to elucidate whether miR-203 interactedwith MIAT and CF6 in MI. Results revealed that MIAT andCF6 expressions were upregulated and that miR-203 wasdownregulated in mouse myocardial tissues after MI, as wellas in hypoxic mouse cardiomyocytes. The overexpressionof MIAT in mouse cardiomyocytes raised CF6 expression,whereas the knockdown of MIAT had the opposite eff ect. Mechanistically, the luciferase reporter and RNA pull-downassays corroborated the binding between miR-203 and CF63′UTR and between miR-203 and MIAT. The simultaneousoverexpression of miR-203 and MIAT restored the reductionof CF6 caused by miR-203 overexpression alone, andthe overexpression of miR-203 diminished the percentage ofinfarct area and the apoptosis of cardiomyocytes in vivo. Our fi ndings corroborate that overexpressing miR-203 alleviatesMI via interacting with MIAT and CF6.