ArticleCardiovascular therapeutics2026
Genetic Evidence Linking Inflammatory Cytokines and Blood Metabolites to Heart Failure Risk.
Article in Cardiovascular therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Genetic Evidence Linking Inflammatory Cytokines and Blood Metabolites to Heart Failure Risk.Cardiovascular therapeutics · 2026Article
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5 authors.
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Abstract
backgroundHeart failure (HF) is a critical condition characterized by the heart's inability to pump blood effectively, leading to significant morbidity and mortality. Inflammation and metabolic disturbances play key roles in its progression. This study is aimed at elucidating the causal relationships between inflammatory cytokines, metabolites, and HF using Mendelian randomization (MR).
methodsA three-step, two-sample MR analysis was performed using genetic data from genome-wide association studies. The study included data on 91 inflammatory cytokines, over 1400 metabolites, and HF cases from the FinnGen project, comprising 29,672 cases and 382,509 controls. Single-nucleotide polymorphisms with significant associations (p < 1 × 10
resultsThe MR analysis identified eight inflammatory cytokines significantly associated with HF risk. Elevated levels of three cytokines (FGF19, MMP-1, and TNF-β) were linked to an increased risk of HF, whereas five cytokines (DNER, IL-10, uPA, TNFSF12, and LIFR) were linked to a decreased risk of HF. Additionally, 12 metabolites were found to be significantly associated with HF, with 6 (2PY, BCG, NAG/NAGal, X-24801, X-21283, and X-22776) enhancing risk and 6 (PC, 3HL, 2-BG, X-23659, X-25422, and X-24546) showing protective effects. Notably, mediation analysis indicated that certain metabolites, X-22776, mediated the effect of uPA on HF.
conclusionsThis study provides novel genetic evidence supporting the causal role of inflammatory cytokines in HF and highlights the mediating role of metabolites. These findings offer new insights into the pathogenesis of HF and suggest potential biomarkers and therapeutic targets for its prevention and treatment.
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