ArticleOxidative medicine and cellular longevity2022
Transcriptomics Coupled to Proteomics Reveals Novel Targets for the Protective Role of Spermine in Diabetic Cardiomyopathy.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Investigating the biomarkers of diabetic-cardiomyopathy with the high mobility group box-1 as a potential anti-inflammatory therapeutic target: Systematic Review and meta-analysis.Frontiers in endocrinology · 2025Pooled it
- Integrated transcriptomic and proteomic profiling implicates prostaglandin-nitric oxide network dysregulation in uterine microcirculatory impairment in primary dysmenorrhea.Frontiers in immunology · 2026Article
- Effect of autophagy-related (Atg) protein 5 on mouse epididymal sperm maturation.Journal of assisted reproduction and genetics · 2026Article
- Multi-omics analysis of diabetic cardiomyopathy pathogenesis using a type 2 diabetic Zucker diabetic fatty rat model.Scientific reports · 2025Article
- Emerging Insights into the Relationship Between Amino Acid Metabolism and Diabetic Cardiomyopathy.Biomolecules · 2025Review
- Transcriptomic and Proteomic Profiling of Rabbit Kidney Cells Infected with Equine Herpesvirus 8.Viruses · 2025Article
- Murine Model Insights: Identifying Dusp15 as a Novel Biomarker for Diabetic Cardiomyopathy Uncovered Through Integrated Omics Analysis and Experimental Validation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Molecular mechanisms of diabetic heart disease: Insights from transcriptomic technologies.Diabetes & vascular disease researchReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Diabetic cardiomyopathy (DbCM) is the main complication and the cause of high mortality of diabetes. Exploring the transcriptomics and proteomics of DbCM is of great significance for understanding the biology of the disease and for guiding new therapeutic targets for the potential therapeutic effect of spermine (SPM). Methods and Results: By using a mouse DbCM model, we analyzed the overall transcriptome and proteome of the myocardium, before/after treatment with SPM. The general state and cardiac structure and function changes of each group were also compared. Diabetes induced an increased blood glucose and serum triglyceride content, a decreased body weight, serum insulin level, and cardiac function-related indexes, accompanied by disrupted myocardial tissue morphology and ultrastructure damage. Using RNA sequencing (RNA-seq), we identified thousands of differentially expressed genes (DEGs) in DbCM with or without SPM treatment. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis demonstrated that the DEGs were significantly enriched in lipid metabolism and amino acid metabolism pathways. Specifically, quantitative real-time PCR (qRT-PCR) confirmed that SPM protected DbCM by reversing the expressions of lipid metabolism and amino acid metabolism-related genes, including Alox15, Gm13033, pla2g12a, Ptges, Pnpla2, and Acot1. To further reveal the pathogenesis of DbCM, we used proteome-based data-independent acquisition (DIA) and identified 139 differentially expressed proteins (DEPs) with 67 being upregulated and 72 being downregulated in DbCM. Venn intersection analysis showed 37 coexpressed genes and proteins in DbCM, including 29 upregulation and 8 downregulation in DbCM. In the protein-protein interaction (PPI) network constructed by the STRING database, the metabolism-related coexpressed genes and proteins, such as Acot2, Ephx2, Cyp1a1, Comt, Acox1, Hadhb, Hmgcs2, Acot1, Inmt, and Cat, can interact with the identified DEGs and DEPs. Conclusion: The biomarkers and canonical pathways identified in this study may hold the key to understand the mechanisms of DbCM pathobiology and provide new targets for the therapeutic effect of SPM against DbCM by targeting lipid and amino acid metabolism pathways.
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