ArticlemSystems2025
The potential mechanisms of reciprocal regulation of gut microbiota-liver immune signaling in metabolic dysfunction-associated steatohepatitis revealed in multi-omics analysis.
Article in mSystems, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- Anti-obesity mechanisms of adzuki bean saponin: a multi-omics and experimental study.NPJ science of food · 2026Article
- Regulation of immune tolerance in hepatocellular carcinoma by liver diseases: a review.Infectious agents and cancer · 2026Review
- Molecular mechanisms in endometriosis: linking JAK/STAT pathway, ferroptosis, and microbial dysbiosis.Molecular biology reports · 2026Review
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Authors and funding
10 authors.
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Abstract
As a commonly known aggressive liver-related manifestation within the spectrum of metabolic syndrome with a significant risk of progressing to cirrhosis and hepatocellular carcinoma, metabolic dysfunction-associated steatohepatitis (MASH) is closely intertwined with obesity, insulin resistance, and dyslipidemia. Although the gut microbiota is implicated in MASH progression, the underlying mechanisms require further investigation. In this study, we sought to combine the analysis of the liver transcriptome, circulating metabolome, and gut microbiota to investigate the potential molecular mechanisms underlying the reciprocal regulation between gut microbiota and liver immune signaling. We utilized a high-fat and methionine/choline-deficient diet (HFMCD)-induced MASH model in a db/db mouse. Following annotation analysis using KEGG and Metorigin, a comprehensive correlation analysis was conducted among these genes and specific metabolites (such as L-glutamine, isocitric acid, putrescine, pyroglutamic acid, rhamnose) and gut microbiota genera (
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