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HLA-B and TIMP1 as hub genes of the ventricular remodeling caused by hypertension
Gai-Feng Hu1, Ling-Bing Meng2, Jianyi Li3,4
1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, National Clinical Research Center for Cardiovascular Diseases, Chaoyang 100029, Beijing, China.
Insights
Hypertension-induced ventricular remodeling involves myocardial fibrosis. Researchers found HLA-B and TIMP1 gene expression is higher in patients with heart failure with preserved ejection fraction (HFpEF), suggesting they are key targets for treatment.
Area of Science:
- Cardiovascular Biology
- Molecular Mechanisms of Disease
- Genomics and Bioinformatics
Background:
- Myocardial fibrosis is a key pathological change in hypertensive ventricular remodeling, contributing to cardiovascular disease.
- The precise molecular mechanisms driving this remodeling process remain largely unknown.
Purpose of the Study:
- To elucidate the molecular mechanisms of myocardial fibrosis in hypertensive ventricular remodeling.
- To identify key genes and potential therapeutic targets for hypertensive heart disease.
Main Methods:
- Bioinformatics analysis including Weighted Gene Co-expression Network Analysis (WGCNA) to identify hub genes.
- Construction of a competing endogenous RNA (ceRNA) network.
- Quantitative real-time PCR (RT-qPCR) to validate gene expression.
- Logistic regression and Receiver Operating Characteristic (ROC) curve analysis.
Main Results:
- Bioinformatics identified HLA-B and TIMP1 as significant hub genes in myocardial fibrosis.
- WGCNA indicated HLA-B's role in ventricular remodeling (correlation coefficient = 0.67).
- RT-qPCR confirmed significantly elevated expression of HLA-B and TIMP1 in patients with hypertensive left ventricular remodeling (HLVR) compared to controls.
Conclusions:
- HLA-B and TIMP1 are implicated in the pathogenesis of hypertensive left ventricular remodeling.
- These genes represent promising novel targets for the diagnosis and treatment of HLVR.
Rationale:
Myocardial fibrosis is an important pathological change that occurs during ventricular remodeling in patients with hypertension and is an important pathophysiological basis of cardiovascular disease. However, the molecular mechanism underlying this ventricular remodeling is unclear.
Methods:
Bioinformatics analysis identified HLA-B and TIMP1 as hub genes in the process of myocardial fibrosis. Expression and correlation analyses of significant hub genes with ventricular remodeling were performed. Weighted gene co-expression network analysis (WGCNA) was performed to verify the role of HLA-B. ceRNA network was constructed to identify the candidate molecule drugs. Receiver operating characteristic (ROC) curves were analyzed.
Results:
RT-qPCR was performed to verify the roles of HLA-B and TIMP1 in seven control individuals with hypertension and seven patients with hypertension and ventricular remodeling. The WGCNA showed that HLA-B was in the brown module and the correlation coefficient between HLA-B and ventricular remodeling was 0.67. Based on univariate logistic proportional regression analysis, HLA-B influences ventricular remodeling (P<0.05). RT-qPCR showed that the relative expression levels of HLA-B and TIMP1 were significantly higher in HLVR samples compared with their expression in the control group.
Conclusions:
HLA-B and TIMP1 might provide novel research targets for the diagnosis and treatment of HLVR.
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