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Updated: Jan 30, 2026
Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
Published on: November 29, 2024
Identification of Core Gene Biomarkers in Patients with Diabetic Cardiomyopathy
Ning Li1, Haiming Wu1, Rongxin Geng2
1Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Hubei Key Laboratory of Cardiology, Wuhan, China.
Insights
Diabetic cardiomyopathy (DCM) involves inflammation and mitochondrial dysfunction. Restoring SOCS3 levels may reverse high glucose-induced heart damage, offering new therapeutic targets for DCM.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genomics
Background:
- Diabetic cardiomyopathy (DCM) is a serious diabetes complication with high mortality.
- The precise molecular mechanisms driving DCM remain largely unknown.
- Identifying key molecular players is crucial for effective DCM diagnosis and treatment.
Purpose of the Study:
- To identify differentially expressed genes (DEGs) and pathways involved in DCM.
- To explore the roles of specific genes, such as IL6 and SOCS3, in DCM pathogenesis.
- To investigate the therapeutic potential of modulating SOCS3 in DCM.
Main Methods:
- Analysis of gene expression data (GSE26887) from DCM patients and controls.
- Gene Ontology (GO), KEGG pathway, and protein-protein interaction (PPI) network analyses.
- Validation using quantitative real-time PCR (qPCR) and Western blot in mouse models and cell cultures.
Main Results:
- Identified 236 DEGs, highlighting roles for inflammation, immune disorders, metabolic disturbance, and mitochondrial dysfunction.
- IL6 identified as a key upregulated hub gene; SOCS3 identified as a top hub gene.
- Reduced SOCS3 and activated STAT3 observed in DCM models; SOCS3 overexpression ameliorated high glucose-induced cardiac damage.
Conclusions:
- Inflammation, metabolic issues, and mitochondrial dysfunction are key in DCM development.
- SOCS3 acts as a protective factor, and its downregulation contributes to DCM.
- Targeting SOCS3 presents a promising therapeutic strategy for diabetic cardiomyopathy.
Abstract:
Diabetic cardiomyopathy (DCM) is a disorder of the myocardium in diabetic patients, which is one of the critical complications of diabetes giving rise to an increased mortality. However, the underlying mechanisms of DCM remain incompletely understood presently. This study was designed to screen the potential molecules and pathways implicated with DCM. GSE26887 involving 5 control individuals and 7 DCM patients was selected from the GEO database to identify the differentially expressed genes (DEGs). DAVID was applied to perform gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. A protein-protein interaction (PPI) network was also constructed to visualize the interactions among these DEGs. To further validate significant genes and pathways, quantitative real-time PCR (qPCR) and Western blot were performed. A total of 236 DEGs were captured, including 134 upregulated and 102 downregulated genes. GO, KEGG, and the PPI network disclosed that inflammation, immune disorders, metabolic disturbance, and mitochondrial dysfunction were significantly enriched in the development of DCM. Notably, IL6 was an upregulated hub gene with the highest connectivity degree, suggesting that it may interact with a great many molecules and pathways. Meanwhile, SOCS3 was also one of the top 15 hub genes in the PPI network. Herein, we detected the protein level of STAT3 and SOCS3 in a mouse model with DCM. Western blot results showed that the protein level of SOCS3 was significantly lower while phosphorylated-STAT3 (P-STAT3) was activated in mice with DCM. In vitro results also uncovered the similar alterations of SOCS3 and P-STAT3 in cardiomyocytes and cardiac fibroblasts induced by high glucose (HG). However, overexpression of SOCS3 could significantly reverse HG-induced cardiomyocyte hypertrophy and collagen synthesis of cardiac fibroblasts. Taken together, our analysis unveiled potential biomarkers and molecular mechanisms in DCM, which could be helpful to the diagnosis and treatment of DCM.
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