ArticleFrontiers in endocrinology2024
Causal relationships between the gut microbiota, inflammatory cytokines, and alcoholic liver disease: a Mendelian randomization analysis.
Article in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Dietary Isorhamnetin Alleviates Alcoholic Liver Injury in Mice by Regulating Gut Microbiota via the Gut-Liver Axis.Nutrients · 2026Article
- Gut Microbiota and Ageing: A Critical Crosstalk in Alcohol-Related Liver Disease.Microorganisms · 2026Review
- The role of Traditional Chinese Medicine in the management of liver disease: targeting gut microbiome.Chinese medicine · 2026Review
- High-fat diet-driven gut microbial sphingolipid metabolic reprogramming is associated with stress susceptibility in CUMS rats.Frontiers in microbiology · 2026Article
- Prospects of Mendelian randomization in hepatology: a comprehensive literature review with practice guidance.Clinical and molecular hepatology · 2025Review
- Causal Associations of Smoking, Alcohol, Obesity, Sedentary Behavior, Hypertension, and Hyperglycemia With Retinal Vein Occlusion: A Mendelian Randomization Study.Current genomics · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
Objective: Previous studies have suggested a potential association between gut microbiota and the development of alcohol-related liver disease (ALD). However, the causal relationship between gut microbiota and ALD, as well as the role of inflammatory cytokines as mediators, remains unclear. This study aims to explore the causal relationship between gut microbiota and ALD using Mendelian randomization (MR) methods, and to analyze the mediating role of inflammatory cytokines. Methods: Gut microbiota, 91 inflammatory cytokines, and ALD were identified from summary data of large-scale genome-wide association studies (GWAS). MR was employed to investigate the causal relationship between gut microbiota, cytokines, and ALD, with the inverse variance-weighted method (IVW) as the primary statistical approach. Additionally, we examined whether inflammatory cytokines act as mediating factors in the pathway from gut microbiota to ALD. Results: The IVW results confirmed two positive and one negative causal effect between genetic liability in the gut microbiota and ALD. Conclusion: In conclusion, our study supports a causal relationship among gut microbiota, inflammatory cytokines and ALD, with inflammatory cytokines potentially acting as mediating factors in the pathway from gut microbiota to ALD.
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