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Exploring the impact of metabolites function on heart failure and coronary heart disease: insights from a Mendelian
Vicheth Virak1, Pengkhun Nov2, Deshu Chen1
1Department of Cardiology, Laboratory of Heart Center, Zhujiang Hospital, Southern Medical University Guangzhou, Guangdong, The People's Republic of China.
Insights
Metabolite functions impact heart failure (HF) and coronary heart disease (CHD). Specific metabolites like erucate and γ-glutamyl glycine, and imbalanced ratios, increase cardiovascular risk, warranting further mechanistic study.
Area of Science:
- Cardiovascular Disease Epidemiology
- Metabolomics
- Genetic Epidemiology
Background:
- Heart failure (HF) and coronary heart disease (CHD) are leading global health burdens.
- Traditional risk factors are well-studied, but the role of metabolite functions in cardiovascular disease (CVD) development remains less understood.
- Mendelian randomization (MR) offers a powerful approach to investigate causal relationships between metabolites and CVD.
Purpose of the Study:
- To investigate the causal impact of metabolite functions on the risk of heart failure (HF) and coronary heart disease (CHD).
- To identify specific metabolic phenotypes associated with increased risk of these cardiovascular conditions.
Main Methods:
- Utilized a Mendelian randomization (MR) approach to assess causal effects.
- Employed genetic variants associated with metabolite levels as instrumental variables.
- Integrated comprehensive genetic and phenotypic data from diverse large-scale cohorts and GWAS.
Main Results:
- Identified ten significant metabolic cell phenotypes influencing HF and CHD risk among 61 assessed.
- Found that elevated erucate (22:1n9), elevated γ-glutamyl glycine, and elevated 7-methylguanine increased risk.
- Observed that lower α-tocopherol and an imbalanced citrulline-to-ornithine ratio were associated with increased cardiovascular risk.
- Results were consistent across populations and robust to sensitivity analyses.
Conclusions:
- This MR study provides robust evidence for the influence of specific metabolite functions on HF and CHD.
- Highlights the potential of certain metabolites as novel risk factors for cardiovascular diseases.
- Further research into the underlying mechanisms is crucial for developing targeted therapeutic strategies.
Background:
Heart failure (HF) and coronary heart disease (CHD) are major causes of morbidity and mortality worldwide. While traditional risk factors such as hypertension, diabetes, and smoking have been extensively studied, the role of metabolite functions in the development of these cardiovascular conditions has been less explored. This study employed a Mendelian randomization (MR) approach to investigate the impact of metabolite functions on HF and CHD.
Methods:
To assess the causal impacts of specific metabolite risk factors on HF and CHD, this study utilized genetic variants associated with these factors as instrumental variables. Comprehensive genetic and phenotypic data from diverse cohorts, including genome-wide association studies (GWAS) and cardiovascular disease registries, were incorporated into the research.
Results:
Our results encompass 61 metabolic cell phenotypes, with ten providing strong evidence of the influence of metabolite functions on the occurrence of HF and CHD. We found that elevated levels of erucate (22:1n9), lower levels of α-tocopherol, an imbalanced citrulline-to-ornithine ratio, elevated γ-glutamyl glycine levels, and elevated 7-methylguanine levels independently increased the risk of these cardiovascular conditions. These findings were consistent across different populations and robust to sensitivity analyses.
Conclusion:
This MR study provides valuable insights into the influence of metabolite functions on HF and CHD. However, further investigation is needed to fully understand the precise mechanisms by which these metabolite factors contribute to the onset of these conditions. Such research could pave the way for the development of targeted therapeutic strategies.
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