Diabetic　cardiomyopathy　(DCM)　is　a　common　form　of　cardiomyopathy　that　affects　the　cardiac　muscle.　It　can　lead　to　heart　failure　and　threaten　the　life　of　human.　Neuregulin　4　(NRG4)　is　a　novel　adipose　factor　released　from　brown　adipose　tissues　and　is　considered　to　play　an　important　role　in　metabolism,　and　affects　the　diabetic　cardiomyopathy.　N6-Methyladenosine　(m6A)　modification　has　been　implicated　in　many　bioprocesses.　So　we　aim　to　explore　the　role　of　methyltransferase　14　(METTL14)　and　NRG4　in　the　progression　of　DCM.　The　high-glucose　(HG)　could　increase　the　expression　of　NRG4.　In　HG-induced　H9C2　cells,　the　up-regulated　NRG4　promoted　the　cell　proliferation　and　GSH　levels,　and　suppressed　the　cell　apoptosis,　inflammation　factors　(IL-1　beta　and　IL-6),　and　Fe2+　and　ROS　levels.　The　RMbase　database,　SRAMP　website,　and　RMvar　database　predicted　that　NRG4　had　m6A　modification　site.　Western　blot　assay　demonstrated　that　OE-METTL14　promoted　NRG4　expression.　METTL3　could　bind　to　NRG4.　Besides,　METTL14　and　IGF2BP1　positively　regulated　NRG4　by　increasing　its　mRNA　stability.　In　HG-induced　H9C2　cells,　METTL14　promoted　the　NRG4　levels　and　cell　proliferation　and　retarded　the　cell　apoptosis,　inflammation　and　ferroptosis　via　facilitating　expression　of　NRG4.　Besides,　the　METTL14　overexpression　could　increase　the　expression　of　nuclear　factor　erythroid　2-related　factor　2　(NRF2),　solute　carrier　family　7　member　11　(SLC7A11),　and　glutathione　peroxidase　4　(GPX4)　in　HG-induced　H9C2　cells.　METTL14　curbs　the　progression　of　DCM　via　enhancing　the　m6A　methylation　of　NRG4　in　HG-induced　H9C2　cells,　which　can　help　extend　our　understanding　on　the　epigenetic　regulation　of　ferroptosis　in　DCM　progression.