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This study aimed to examine the functional role of microRNA-20 (miR-20) and its potential target,Kir6.1,in ischemic myocardiocytes.The expression of miR-20 was detected by real-time PCR.Myocardiocytes were stained with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) reagent for apoptosis evaluation.West blotting was used to detect the Kit6.1 protein in ischemic myocardiocytes transfected with miR-20 mimics or inhibitors.Luciferase reporter gene assay was performed to confirm the targeting effect of miR-20 on KCNJ8.The results showed that miR-20 was remarkably down-regulated,while the KATP subunit Kir6.1 was significantly up-regulated,during myocardial ischemia.The miR-20 overexpression promoted the apoptosis of ischemic myocardiocytes,but showed no such effect on normal cells.Under ischemic condition,myocardiocytes transfected with miR-20 mimics expressed less Kir6.1.On the contrary,inhibiting miR-20 increased the expression of Kir6.1 in the cells.Co-transfection of miR-20 mimics with the KCNJ8 3’-UTR plasmid into HEK293 cells consistently produced less luciferase activity than transfection of the plasmid alone.It was concluded that miR-20 may regulate myocardiac ischemia by targeting KATP subunit Kir6.1 to accelerate the cell apoptosis.Therefore miR-20 may serve as a therapeutic target for myocardial ischemic disease.