〔Abstract〕 Objective To investigate the effect and mechanism of long non-coding RNA RMRP(LncRNA RMRP) on oxygen-glucose deprivation/reperfusion(OGD/R)-induced ferroptosis in mouse HL-1 cardiomyocytes by regulating miR-766-5p. Methods HL-1 cells were cultured in vitro, and OGD/R models were established. The expression levels of LncRNA RMRP in HL-1 cells at various reperfusion time points were subsequently quantified using qRT-PCR. The LncRNA RMRP small RNA interference fragment(si-RMRP) and its corresponding negative control(si-NC), as well as the miR-766-5p inhibitor and its respective negative control(inhibitor-NC), were transfected into HL-1 cells. Subsequently, the cells were subjected to OGD/R treatment. CCK-8 assay was employed to evaluate cell viability. Assay kits were employed to measure the levels of lactate dehydrogenase(LDH) in the cell supernatant, as well as the intracellular levels of malondialdehyde(MDA), superoxide dismutase(SOD), glutathione(GSH), and ferrous ion(Fe2+). qRT-PCR analysis was conducted to assess the expression levels of LncRNA RMRP and miR-766-5p. Western blot analysis was conducted to assess the expression levels of proteins associated with ferroptosis including GPX4, SLC7A11, and FTH1. Dual-luciferase reporter assays were performed to investigate the sponge adsorption relationship between LncRNA RMRP and miR-766-5p. Results As reperfusion time extended, the expression level of LncRNA RMRP in cells progressively increased(P2+ levels within the cells, and decreased the activities of SOD and GSH in cells(P2+ levels within the cells, and promoting SOD and GSH activities in cells(P