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Exploring novel biomarkers in dilated cardiomyopathy‑induced heart failure by integrated analysis and in vitro
Lei Zhou1,2, Fei Peng1, Juexing Li1,2
1Department of Cardiology, Jinshan Hospital of Fudan University, Shanghai 201508, P.R. China.
Insights
Researchers identified novel biomarkers for dilated cardiomyopathy (DCM)-induced heart failure (HF). Key genes like SERPINA3 and MYH6 show promise for improved diagnosis and treatment strategies in HF patients.
Area of Science:
- Cardiovascular Biology
- Genomics
- Biomarker Discovery
Background:
- Heart failure (HF) remains a significant global health issue, necessitating advanced therapeutic approaches.
- Dilated cardiomyopathy (DCM) is a primary contributor to HF development and progression.
- Current diagnostic and treatment strategies for DCM-induced HF require enhancement.
Purpose of the Study:
- To identify novel biomarkers and biological pathways for improved diagnosis and treatment of DCM-induced HF.
- To utilize weighted gene co-expression network analysis (WGCNA) for comprehensive gene expression profiling.
- To pinpoint key genes and pathways implicated in the pathogenesis of DCM-induced HF.
Main Methods:
- Weighted gene co-expression network analysis (WGCNA) was employed to identify gene modules associated with DCM-induced HF.
- Differential gene expression analysis was performed to pinpoint key therapeutic targets.
- Immune cell infiltration analysis and reverse transcription-quantitative PCR (RT-qPCR) were used for validation.
Main Results:
- WGCNA identified 24 gene modules correlated with DCM-induced HF, with the blue module showing the strongest association (r=0.91).
- Enriched pathways included AGE-RAGE signaling, p53 and MAPK signaling, adrenergic signaling, JAK-STAT, and cGMP/PKG signaling.
- Eight key genes (SMOC2, SERPINA3, MYH6, S100A9, TUBA3E, TUBA3D, LYVE1, PLCE1) were identified as potential therapeutic targets.
- Increased naive B cells and CD4-activated memory T cells were observed in DCM-induced HF tissues.
- RT-qPCR validated the expression of SERPINA3, MYH6, S100A9, LYVE1, and PLCE1 in doxorubicin-treated cardiomyocytes.
Conclusions:
- SERPINA3, MYH6, S100A9, LYVE1, and PLCE1 are identified as potential key genes involved in DCM-induced HF.
- These genes and associated pathways offer novel targets for therapeutic intervention and diagnostic strategies.
- Further research is warranted to fully elucidate the role of these genes in HF pathogenesis.
Abstract:
Despite the availability of several effective and promising treatment methods, heart failure (HF) remains a significant public health concern that requires advanced therapeutic strategies and techniques. Dilated cardiomyopathy (DCM) is a crucial factor that contributes to the development and deterioration of HF. The aim of the present study was to identify novel biomarkers and biological pathways to enhance the diagnosis and treatment of patients with DCM-induced HF using weighted gene co-expression network analysis (WGCNA). A total of 24 co-expressed gene modules connected with DCM-induced HF were obtained by WGCNA. Among these, the blue module had the highest correlation with DCM-induced HF (r=0.91; P<0.001) and was enriched in the AGE-RAGE signaling pathway in diabetic complications, the p53 and MAPK signaling pathway, adrenergic signaling in cardiomyocytes, the Janus kinase-STAT signaling pathway and cGMP/PKG signaling. Eight key genes, including secreted protein acidic and rich in cysteine-related modular calcium-binding protein 2 (SMOC2), serpin family A member 3 (SERPINA3), myosin heavy chain 6 (MYH6), S100 calcium binding protein A9 (S100A9), tubulin α (TUBA)3E, TUBA3D, lymphatic vessel endothelial hyaluronic acid receptor 1 (LYVE1) and phospholipase C ε1 (PLCE1), were selected as the therapeutic targets of DCM-induced HF based on WGCNA and differentially expressed gene analysis. Immune cell infiltration analysis revealed that the proportion of naive B cells and CD4-activated memory T cells was markedly upregulated in DCM-induced HF tissues compared with tissues from healthy controls. Furthermore, reverse transcription-quantitative PCR in AC16 human cardiomyocyte cells treated with doxorubicin showed that among the eight key genes, only SERPINA3, MYH6, S100A9, LYVE1 and PLCE1 exhibited expression levels identical to those revealed by bioinformatics analysis, suggesting that these genes may be involved in the development of DCM-induced HF.
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