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N6-methyladenosine(m6A),a methylation in the N6 position of adenosine especially in the mRNA,exerts diverse physiological and pathological functions.However,the precise role of m6A methy-lation in hypoxic preconditioning(HPC)is still unknown.Here,we observed that HPC treatment protected H9c2 cells against H2O2-induced injury,upregulated the m6A level in the total RNA and the expression of methyltransferase like 3(METTL3),methyltransferase like 14(METTL14),and long noncoding RNA(IncRNA)H19.Either knockdown of METTL3 or METTL14 notably reversed the HPC-induced enhancement of cell viability,anti-apoptosis ability,and H19 expression.Methy-lated RNA immunoprecipitation(IP)indicated that knockdown of METTL3 or METTL14 decreased m6A level in the IncRNA H19.Gain-of-function assay demonstrated that H19 overexpression could partially rescue the decreased protection mediated by METTL3 or METTL14 knockdown in HPC-treated H9c2 cells.RNA binding protein immunoprecipitation(RIP)assay showed that METTL3 and METTL14 could directly bind with H19.Our study identified a novel pattern of posttranscriptional regulation in HPC treatment.Since METTL3,METTL14,and IncRNA H19 were involved in HPC pro-tection,they could be considered as potential biomarkers and therapeutic targets in HPC-derived cardiac rehabilitation and therapeutic approaches.