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Exploring the Role of Obesity in Dilated Cardiomyopathy Based on Bio-informatics Analysis
Xuehua Wang1,2,3, Wei Liu1,2,3,4, Huili Li1,2,3
1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Insights
Obesity increases dilated cardiomyopathy (DCM) risk by disrupting the immune environment, promoting oxidative stress, and causing fibrosis. Key genes like KLHL29 and HTRA1 are implicated in this process.
Area of Science:
- Cardiovascular Biology
- Obesity Research
- Genomics
Background:
- Obesity is a significant risk factor for cardiovascular disease (CVD), including an elevated risk of dilated cardiomyopathy (DCM).
- Understanding the biological mechanisms linking obesity to DCM is crucial for public health.
- Recent studies highlight the association between obesity and increased DCM incidence.
Purpose of the Study:
- To investigate the underlying biological role of obesity in increasing the risk of dilated cardiomyopathy (DCM).
- To identify common genes and pathways affected by both obesity and DCM.
- To explore the relationship between key genes and immune cell composition in obesity-related DCM.
Main Methods:
- Utilized Gene Expression Omnibus (GEO) datasets (GSE120895, GSE19303, GSE2508) for differential gene expression analysis.
- Performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses.
- Employed LASSO algorithm for key gene identification and ROC curves for validation, alongside CIBERSORT for immune cell analysis and Spearman's correlation for gene-immune cell interactions.
Main Results:
- Common genes between obesity and DCM were enriched in pathways including transforming growth factor-beta (TGF-β), fibrillar collagen, NADPH oxidase activity, and hormone signaling.
- Obesity and DCM exhibited disordered immune environments, with obesity showing more significant alterations.
- Identified key genes NOX4, CCDC80, COL1A2, HTRA1, and KLHL29, with KLHL29 correlating with T cells/M2 macrophages and HTRA1 with plasma cells.
Conclusions:
- Obesity disrupts the immune micro-environment, promotes oxidative stress, and increases myocardial fibrosis, contributing to ventricular remodeling and DCM risk.
- Bio-informatics analysis suggests key genes KLHL29 and HTRA1 play critical roles in obesity-related DCM.
- These findings provide insights into the molecular mechanisms underlying obesity-induced DCM.
Abstract:
(1) Background: Obesity is a major risk factor for cardiovascular disease (CVD), contributing to increasing global disease burdens. Apart from heart failure, coronary artery disease, and arrhythmia, recent research has found that obesity also elevates the risk of dilated cardiomyopathy (DCM). The main purpose of this study was to investigate the underlying biological role of obesity in increasing the risk of DCM. (2) Methods: The datasets GSE120895, GSE19303, and GSE2508 were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were analyzed using GSE120895 for DCM and GSE2508 for obesity, and the findings were compiled to discover the common genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted for the common genes in RStudio. In addition, CIBERSORT was used to obtain the immune cellular composition from DEGs. The key genes were identified in the set of common genes by the least absolute shrinkage and selection operator (LASSO) algorithm, the prognostic risk models of which were verified by receiver operator characteristic (ROC) curves in GSE19303. Finally, Spearman's correlation was used to explore the connections between key genes and immune cells. (3) Results: GO and KEGG pathway enrichment analyses showed that the main enriched terms of the common genes were transforming growth factor-beta (TGF-β), fibrillar collagen, NADPH oxidase activity, and multiple hormone-related signaling pathways. Both obesity and DCM had a disordered immune environment, especially obesity. The key genes NOX4, CCDC80, COL1A2, HTRA1, and KLHL29 may be primarily responsible for the changes. Spearman's correlation analysis performed for key genes and immune cells indicated that KLHL29 closely correlated to T cells and M2 macrophages, and HTRA1 very tightly correlated to plasma cells. (4) Conclusions: Bio-informatics analyses performed for DCM and obesity in our study suggested that obesity disturbed the immune micro-environment, promoted oxidative stress, and increased myocardial fibrosis, resulting in ventricular remodeling and an increased risk of DCM. The key genes KLHL29 and HTRA1 may play critical roles in obesity-related DCM.
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