ArticlePharmacogenomics and personalized medicine2021
Metabolic Processes are Potential Biological Processes Distinguishing Nonischemic Dilated Cardiomyopathy from Ischemic Cardiomyopathy: A Clue from Serum Proteomics.
Article in Pharmacogenomics and personalized medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- VAP1 promotes cardiac fibrosis by enabling PDGFR signaling in myofibroblasts.Experimental & molecular medicine · 2026Article
- Deregulated nutrient response in ttntv cardiomyopathy can be repaired via Erk inhibition for cardioprotective effects.Journal of molecular and cellular cardiology · 2025Article
- 401-Gene Signature of Myocardial Dysfunction in Human Heart Failure: A Transcriptomic Analysis.Cureus · 2025Article
- Integrative proteomic and metabolomic elucidation of cardiomyopathy with in vivo and in vitro models and clinical samples.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Calsyntenin-1 Promotes Doxorubicin-induced Dilated Cardiomyopathy in Rats.Cardiovascular drugs and therapy · 2024Article
- Potential mechanisms underlying podophyllotoxin-induced cardiotoxicity in male rats: toxicological evidence chain (TEC) concept.Frontiers in pharmacology · 2024Article
- Integrated genomic analysis defines molecular subgroups in dilated cardiomyopathy and identifies novel biomarkers based on machine learning methods.Frontiers in genetics · 2023Article
- Mitochondrial Metabolism in Myocardial Remodeling and Mechanical Unloading: Implications for Ischemic Heart Disease.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemic cardiomyopathy (ICM) and nonischemic dilated cardiomyopathy (DCM) are the two most common causes of heart failure. However, our understanding of the specific proteins and biological processes distinguishing DCM from ICM remains insufficient. MATERIALS AND
methodsThe proteomics analyses were performed on serum samples from ICM (n=5), DCM (n=5), and control (n=5) groups. Proteomics and bioinformatics analyses, including weighted gene co-expression network analysis (WGCNA) and gene set enrichment analysis (GSEA), were performed to identify the hub circulating proteins and the hub biological processes in ICM and DCM.
resultsThe analysis of differentially expressed proteins and WGCNA identified the hub circulating proteins in ICM (GAPDH, CLSTN1, VH3, CP, and ST13) and DCM (one downregulated protein, FGG; 18 upregulated proteins, including HEL-S-276, IGK, ALDOB, HIST1H2BJ, HEL-S-125m, RPLP2, EL52, NCAM1, P4HB, HEL-S-99n, HIST1H4L, HIST2H3PS2, F8, ERP70, SORD, PSMA3, PSMB6, and PSMA6). The mRNA expression of the heart specimens from GDS651 validated that ALDOB, GAPDH, RPLP2, and IGK had good abilities to distinguish DCM from ICM. In addition, GSEA results showed that cell proliferation and differentiation were the hub biological processes related to ICM, while metabolic processes and cell signaling transduction were the hub biological processes associated with DCM.
conclusionThe present study identified five dysregulated hub circulating proteins among ICM patients and 19 dysregulated hub circulating proteins among DCM patients. Cell proliferation and differentiation were significantly enriched in ICM. Metabolic processes were strongly enhanced in DCM and may be used to distinguish DCM from ICM.
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