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Published on: June 10, 2025
The Bioinformatical Identification of Potential Biomarkers in Heart Failure Diagnosis and Treatment
Xiaodong Sheng1, Xiaoqi Jin1, Yanqi Liu1
1Department of Cardiology, Changshu No. 2 People's Hospital, 18 Taishan Road, Changshu, Jiangsu 215000, China.
Insights
This study identifies key genes like COL1A1 and STAT3 that may drive heart failure (HF) progression. These identified genes could serve as crucial biomarkers for diagnosing and treating HF.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- Bioinformatics
Background:
- Heart failure (HF) is a complex condition characterized by impaired cardiac systolic and diastolic function.
- Understanding the underlying molecular mechanisms of HF is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the molecular mechanisms contributing to heart failure (HF).
- To identify potential diagnostic and therapeutic biomarkers for HF.
Main Methods:
- Differential gene expression analysis using the GSE5406 database.
- Gene Ontology (GO), KEGG pathway, and Protein-Protein Interaction (PPI) network analyses were performed on differentially expressed genes (DEGs).
- Cell counting Kit-8 (CCK-8) assays were used to assess the functional impact of hub genes on cell proliferation.
Main Results:
- Identification of 377 upregulated and 461 downregulated DEGs, enriched in pathways related to extracellular matrix organization and gap junctions.
- Seven hub genes (COL1A1, UBB, COL3A1, HSP90AA1, MYC, STAT3, MAPK1) were identified through PPI network analysis.
- Knockdown of STAT3 promoted H9C2 cell proliferation, while UBB knockdown inhibited it, suggesting their roles in cardiac cell function.
Conclusions:
- The identified hub genes (COL1A1, UBB, COL3A1, HSP90AA1, MYC, STAT3, MAPK1) are implicated in promoting heart failure (HF) progression.
- These genes represent potential novel biomarkers for HF diagnosis and therapeutic targets.
Background:
Heart failure (HF) is defined as the inability of the heart's systolic and diastolic function to properly discharge blood flow from the veins to the heart. The goal of our research is to look into the possible mechanism that causes HF.
Methods:
The GSE5406 database was used for screening the differentially expressed genes (DEGs). Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Protein-Protein Interaction (PPI) network were applied to analyze DEGs. Besides, cell counting Kit-8 (CCK-8) was conducted to observe the knockdown effect of hub genes on cell proliferation.
Results:
Finally, 377 upregulated and 461 downregulated DEGs came out, enriched in the extracellular matrix organization and gap junction. According to GSEA results, Hoft cd4 positive alpha beta memory t cell bcg vaccine age 18-45 yo id 7 dy top 100 deg ex vivo up, Sobolev t cell pandemrix age 18-64 yo 7 dy dn, and so on were significantly related to gene set GSE5406. 7 hub genes, such as COL1A1, UBB, COL3A1, HSP90AA1, MYC, STAT3 and MAPK1, were selected from PPI networks. CCK-8 indicated silencing of STAT3 promoted the proliferation of H9C2 cells and silencing of UBB inhibited the proliferation of H9C2 cells.
Conclusion:
Our analysis reveals that COL1A1, UBB, COL3A1, HSP90AA1, MYC, STAT3, and MAPK1 might promote the progression of HF and become the biomarkers for diagnosis and treatment of HF.
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