ArticleAging2026
Causal effects of inflammation on long-term mortality: A mendelian randomization study.
Article in Aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- A generator-matrix model quantifies the limited contribution of measured biomarkers to human mortality acceleration.medRxiv : the preprint server for health sciences · 2026Article
- Causal Effects of Circulating Inflammatory Proteins on Postmenopausal Atrophic Vaginitis in European Populations: A Mendelian Randomization Study with Transcriptomic Validation.International journal of women's health · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin-6 (IL6) signaling plays a key role in inflammation and cardiovascular disease, but its causal effect on long-term mortality remains unclear. We aimed to assess whether genetically proxied levels of IL6, soluble IL6 receptor (IL6R), C-reactive protein (CRP), and growth differentiation factor-15 (GDF15) exert causal effects on long-term all-cause mortality, and to examine potential opposing effects of IL6 and IL6R.
methodsWe conducted Mendelian randomization (MR) using genome-wide association study instruments from >750,000 individuals. The primary outcome was all-cause mortality over a median follow-up of 11.7 years. Secondary outcomes included cardiovascular events and selected non-cardiovascular conditions. Multiple sensitivity analyses were applied to evaluate robustness and directionality.
resultsGenetically higher IL6R levels were associated with reduced mortality (odds ratio (OR) per 1-SD increase: 0.95; 95% CI: 0.91-0.98,
conclusionsIL6 and IL6R appear to be biologically opposing causal regulators of human survival: IL6 increases, while IL6R reduces mortality through cardiovascular mechanisms. CRP and GDF15 likely reflect disease risk rather than drive it. These results support IL6R antagonism as a potential strategy for cardiovascular disease prevention.
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Registered trials
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