Objective: To perform bioinformatics analysis on the gene chip data of myocardial hypertrophy model-human induced pluripotent stem cell derived cardiomyocytes induced by endothelin-1 (hiPSC-CMs), and to explore the expression profile of long non-coding RNAs (lncRNAs) and competing endogenous RNA (ceRNA) regulatory network. Methods: The gene chip related to cardiac hypertrophy in the Gene Expression Omnibus (GEO) database was screened, and the downloaded original probe matrix information and platform annotation file were preprocessed to obtain the gene expression matrix information. The different biotype attributes were assigned to the genes by using the Practical Extraction and Report Language (Perl), to distinguish lncRNAs from mRNAs. Gene differential expression analysis of lncRNAs and mRNAs was performed using the R language limma package. The microRNAs associated with each lncRNA were predicted using a database downloaded online. On this basis, target genes (mRNAs) of microRNAs were predicted using prediction softwares based on TargetScan, miRDB and miRTarBase. The lncRNA-miRNA-mRNA ceRNA regulatory network was constructed using Cytoscape 3.7.1 software. The Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of target genes from the ceRNA network were performed by the online database DAVID6.8 and the web servers KOBAS3.0. Results: Compared with the control groups, there were 19 lncRNAs and 717 mRNAs expressed differentially in ET1-stimulated hiPSC-CMs with statistical significance, among which 4 lncRNAs up-regulated, 15 lncRNAs down-regulated, 312 mRNAs up-regulated and 405 mRNAs down-regulated. ceRNA regulatory network was constructed successfully, in which lncRNA AC017002 and MIR210HG were up-regulated, LINC00342 was down-regulated. The 3 lncRNAs related closely to 9, 10 and 9 miRNAs, respectively. There were 32 target genes in the network, among which 18 up-regulated and 14 down-regulated. GO enrichment analysis showed that the target genes were significantly enriched to 13 different GO subsets, including cell proliferation, plasma membrane, protein binding and so on. KEGG enrichment analysis found that the target genes were enriched to 20 signaling pathways, including the MAPK signaling pathway, apoptosis, Wnt signaling pathway, JAK-STAT signaling pathway, TNF signaling pathway and so on. Conclusion: Our study constructed the ceRNA network, providing a new perspective for exploring the pathogenic mechanism of lncRNAs involved in cardiac hypertrophy. LncRNAs may affect the pathogenesis of cardiac hypertrophy by regulating in the ceRNA network. In the ceRNA network, up-regulated AC017002 and MIR210HG and down-regulated LINC00342 may regulate the expression level of downstream mRNA by means of competitive “sponge adsorption” of miRNA, so that the expression of AP1, c-MYC and PIM1 were up-regulated, and the expression of ASK1 (MAP3K5), MSK1/2 (RPS6KA5) and SFRP1 were down-regulated. These genes were involved in the pathophysiological process of cardiac hypertrophy through MAPK signaling pathway, apoptosis, Wnt signaling pathway, JAK-STST signaling pathway and TNF signaling pathway. It may become a potential therapeutic target, and the development of drugs that block the above-mentioned lncRNAs and/or downstream target genes may have profound clinical significance in the treatment of cardiac hypertrophy.