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Published on: January 28, 2020
The causal relationship between circulating inflammatory proteins and heart failure: A two-sample Mendelian
Fangxiang Wei1, Haomiao Rui2, Rutao Bian3
1The Second Clinical Medical College of Henan University of Chinese Medicine, Zhengzhou, China.
Insights
This study identified causal links between circulating inflammatory proteins and heart failure types (ICM, DCM, HCM). Findings offer insights into heart failure mechanisms, diagnosis, and potential drug targets for better patient outcomes.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Genetics
Background:
- Heart failure, including ischemic cardiomyopathy heart failure (ICM), dilated cardiomyopathy heart failure (DCM), and hypertrophic cardiomyopathy heart failure (HCM), is a significant global health concern.
- The role of circulating inflammatory proteins in the pathogenesis of different heart failure subtypes is not fully understood.
- Identifying specific inflammatory markers could improve diagnosis, prognosis, and therapeutic strategies.
Purpose of the Study:
- To investigate the causal associations between 91 circulating inflammatory proteins and three major types of heart failure: ICM, DCM, and HCM.
- To uncover potential mechanisms underlying heart failure development and progression.
- To identify novel therapeutic targets and diagnostic biomarkers for heart failure.
Main Methods:
- Utilized Mendelian randomization (MR) analysis, a robust genetic epidemiology method, to assess causal relationships.
- Employed multiple MR methods including inverse-variance weighted, weighted median estimator (WME), weighted mode (WM), and MR-Egger regression.
- Analyzed data from 91 circulating inflammatory proteins in relation to ICM, DCM, and HCM.
Main Results:
- Identified specific inflammatory proteins with causal links to ICM, DCM, and HCM.
- Found positive causal relationships for natural killer cell receptor 2B4, CXCL-6, fibroblast growth factor 5, and interleukin-10 with ICM.
- Reported negative causal relationships for CX3CL-1, C-X-C motif chemokine 9, interleukin-10, leukemia inhibitory factor receptor, and signaling lymphocytic activation molecule with ICM; and identified other proteins associated with DCM and HCM.
Conclusions:
- This study establishes causal relationships between several circulating inflammatory proteins and different heart failure subtypes.
- The findings provide a foundation for understanding heart failure pathogenesis and developing targeted therapies.
- Identified proteins may serve as adjunctive diagnostic markers or therapeutic targets for heart failure management.
Abstract:
This study aims to explore the causal associations of 91 circulating inflammatory proteins with ischemic cardiomyopathy heart failure (ICM), dilated cardiomyopathy heart failure (DCM), and hypertrophic cardiomyopathy heart failure (HCM) to provide new ideas for the study of relevant heart failure mechanisms, adjunctive diagnosis and differentiation, and the clinical application of relevant drug targets. An analysis of the causal relationship between circulating inflammatory proteins and heart failure was conducted via inverse-variance weighted, weighted median estimator (WME), weighted mode (WM), and Mendelian randomization-Egger regression with Mendelian randomization. A Mendelian randomization analysis of 91 circulating inflammatory proteins revealed that natural killer cell receptor 2B4 levels, CXCL-6, fibroblast growth factor 5 levels, and interleukin-10 levels had positive causal relationships with ICM, whereas CX3CL-1, C-X-C motif chemokine 9 levels, interleukin-10 levels, leukemia inhibitory factor receptor levels, and signaling lymphocytic activation molecule levels had negative causal relationships; C-C motif chemokine 20 levels, C-X-C motif chemokine 5 levels, C-X-C motif chemokine 9 levels, fibroblast growth factor 5 levels, and oncostatin-M levels were positively correlated with DCM, whereas eukaryotic translation initiation factor 4E-binding protein 1 levels and Fms-related tyrosine kinase 3 ligand levels were negatively associated with DCM; and the CD40L receptor, Fms-related tyrosine kinase 3 ligand levels, hepatocyte growth factor levels, and sulfotransferase 1A1 levels were negatively associated with HCM. In this study, 9 of the 91 circulating inflammatory proteins were causally related to the ICM (4 positive, 5 negative), 7 were causally related to the DCM (5 positive, 2 negative), and 4 were causally related to the HCM (all negative). This study provides a theoretical foundation for the study of the relevant mechanisms of heart failure, clinical diagnosis, and treatment, as well as potential drug candidates closely related to heart failure.
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