ReviewProbiotics and antimicrobial proteins2026
The Gut-Liver Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Mechanisms, Microbiome Interactions and Therapeutic Targets.
Review in Probiotics and antimicrobial proteins, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Review
- Gut-Liver Axis Mechanisms Underlying Spontaneous Reversal of Liver Fibrosis: A Gut Microbiota-Metabolomics Analysis.Metabolites · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a multifactorial condition in which the gut-liver axis plays a central pathogenic role. While a large body of literature has described associations between gut microbiota alterations and MASLD, a critical synthesis of the mechanistic pathways linking microbial activity to liver injury remains lacking. This review specifically focuses on gut-derived microbial metabolites as key mediators of disease progression. We examine how short-chain fatty acids, bile acids, lipopolysaccharide (LPS), trimethylamine-N-oxide (TMAO) and microbially derived ethanol influence hepatic lipid metabolism, inflammation and fibrogenesis through defined molecular pathways, including FXR signaling, TLR4 activation and immune-metabolic crosstalk. Importantly, we highlight inconsistencies in human microbiome studies, limitations in establishing causality and the challenges in translating preclinical findings into effective therapies. Although microbiome-targeted interventions such as probiotics, bile acid modulators and fecal microbiota transplantation show promise, their clinical efficacy remains variable due to interindividual heterogeneity and lack of mechanistic precision.By integrating current mechanistic evidence with translational insights, this review identifies critical knowledge gaps and proposes future directions for metabolite-focused therapeutic strategies. A more precise understanding of gut-derived signaling pathways will be essential to move from associative microbiome research toward targeted and personalized interventions in MASLD.
Indexed as
Identifiers
42168694What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.