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Figure 1. Biological enrichment and Cu²⁺ ion regulation-related pathway analysis, AGE/RAGE levels in diabetic hearts, and influence of RAGE inhibition on diabetes-instigated alterations in biometric and circulating profiling. (A) GO analysis of DEGs; (B) KEGG analysis of DEGs; (C) GSEA analysis quantifies GOBP: cellular response to Cu²⁺ ion pathway; (D) Crossover of cuproptosis-related genes with DEGs in GSE123975; (E) Levels of 5 cuproptosis DEGs from the intersection; (F) Representative immunofluorescent AGE staining in mouse hearts; (G) RAGE mRNA level in mouse hearts; (H-N) Effect of RAGE inhibition using FPS-ZM1 on diabetes-instigated alterations in biometric and circulating profiling; (H) Body weight; (I) Liver weight; (J) Kidney weight; (K) Blood glucose level; (L) Blood triglyceride; (M) Blood cholesterol; (N) Blood AGEs. Mean ± SEM, n = 6 (A-E), 7 (G) or 10 (H-N) mice per group. Bioinformatic analyses were described in detail in relevant method sections. Data in G were analyzed using two-sided Student’s t-test. Data shown in H-N were analyzed using two-way ANOVA followed by Tukey’s post hoc test, ^*P < 0.05 between labeled groups. AGE: Advanced glycation end products; RAGE: receptor for AGEs; GO: Gene Ontology; DEGs: differentially expressed genes; KEGG: Kyoto Encyclopedia of Genes and Genomes; GSEA: Gene Set Enrichment Analysis; ANOVA: analysis of variance; GOBP: gene ontology biological process; SEM: standard error of the mean.