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Author Spotlight: Integrated Multi-Omics Analysis for Unveiling Multicellular Immune Signatures in Clinical Heart Attack Cohorts

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Causal correlations between inflammatory proteins and heart failure: A two-sample Mendelian randomization analysis.

Xian-Guan Zhu¹, Gui-Qin Liu^1,2, Ya-Ping Peng^1,3

¹Department of Cardiology, Anqing Municipal Hospital, Anqing, China.

ESC Heart Failure

|November 6, 2024

Summary

This study used Mendelian randomization to link inflammation-related proteins to heart failure (HF) risk. Matrix metalloproteinase-1 (MMP-1) and TNF-beta are associated with increased HF risk, while urokinase-type plasminogen activator (uPA) shows a protective effect.

Keywords:

Heart failure Inflammatory proteins Matrix metalloproteinase‐1 Mendelian randomization Meta‐analysis TNF‐beta Urokinase‐type plasminogen activator

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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

Area of Science:

Genetics and Cardiovascular Disease
Inflammation and Immunology
Biomarker Discovery

Background:

Inflammation is a key factor in heart failure (HF) development and progression.
The causal links between specific inflammatory proteins and HF risk are not fully understood.
Identifying these links can reveal new therapeutic targets for HF.

Purpose of the Study:

To investigate the genetically supported causal relationships between inflammation-related proteins and HF risk.
To utilize a two-sample Mendelian randomization (MR) approach for robust analysis.
To identify specific inflammatory proteins that may influence HF development.

Main Methods:

Employed a two-sample Mendelian randomization (MR) analysis using genome-wide association study (GWAS) data.
Utilized data from the SCALLOP Consortium for 91 inflammation-related proteins and large-scale HF GWAS datasets (FinnGen and HERMES).
Selected instrumental variables (IVs) based on established MR assumptions and assessed associations using various statistical methods, including inverse-variance weighted (IVW) and MR-Egger regression.

Main Results:

Identified significant associations between three inflammatory proteins and HF risk.
Matrix metalloproteinase-1 (MMP-1) and TNF-beta showed a positive association with increased HF risk in the FinnGen cohort.
Urokinase-type plasminogen activator (uPA) demonstrated an inverse association, suggesting a protective effect against HF in both FinnGen and HERMES cohorts.

Conclusions:

Provided genetically supported evidence for causal links between specific inflammatory proteins and HF risk.
MMP-1 and TNF-beta may contribute to HF pathogenesis, while uPA might offer a protective role.
These findings suggest that targeting specific inflammatory pathways could be a viable therapeutic strategy for managing HF.