# Research advances on gut microbiota dysbiosis and chronic liver diseases: a review

**Authors:** Guozhen Yang, Jiling Zhu, Minxin Wang, Sha She, Kai Dai

PMC · DOI: 10.3389/fmed.2026.1765047 · 2026-01-28

## TL;DR

This review explores how gut microbiota imbalances are linked to chronic liver diseases and discusses potential treatments like probiotics and dietary changes.

## Contribution

The paper provides a comprehensive synthesis of recent research on gut microbiota's role in chronic liver diseases and novel therapeutic strategies.

## Key findings

- Gut microbiota dysbiosis is linked to chronic liver diseases via the gut-liver axis.
- Microbial imbalance affects liver disease progression through immune and metabolic pathways.
- Therapies like FMT and probiotics show promise in modulating gut microbiota for liver disease management.

## Abstract

The gut microbiota is fundamental to human health, maintaining intricate symbiotic interactions with the host. Accumulating evidence highlights a critical association between gut microbiota dysbiosis and the initiation and progression of chronic liver diseases (CLDs). Particularly hepatitis B virus (HBV)/hepatitis C virus (HCV) infection, alcoholic liver disease (ALD), metabolic-associated steatotic liver disease (MASLD), and cirrhosis. This microbial imbalance may contribute to the progression of CLDs primarily via the “gut-liver axis,” the mechanisms involve gut barrier dysfunction, abnormal immune regulation, and metabolic alterations. This review synthesizes cutting-edge research on the interplay between gut dysregulation and CLDs, elaborating molecular mechanistic pathways including the TLR4/NF-κB signaling pathway, AMPK pathway, and farnesoid X receptor (FXR)-mediated bile acid signaling. Additionally, it discusses clinically oriented therapeutic strategies targeting microbiota modulation, including probiotics, fecal microbiota transplantation (FMT), and personalized dietary interventions, offering innovative insights for the prevention and management of chronic liver diseases.

## Linked entities

- **Proteins:** TLR4 (toll like receptor 4), NFKB1 (nuclear factor kappa B subunit 1), PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1), NR1H4 (nuclear receptor subfamily 1 group H member 4)
- **Diseases:** hepatitis B virus infection (MONDO:0005344), hepatitis C virus infection (MONDO:0005231), alcoholic liver disease (MONDO:0043693), cirrhosis (MONDO:0005155)

## Full-text entities

- **Genes:** TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, PRKAA2 (protein kinase AMP-activated catalytic subunit alpha 2) [NCBI Gene 5563] {aka AMPK, AMPK2, AMPKa2, PRKAA}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, NR1H4 (nuclear receptor subfamily 1 group H member 4) [NCBI Gene 9971] {aka BAR, FXR, HRR-1, HRR1, PFIC5, RIP14}
- **Diseases:** cirrhosis (MESH:D005355), CLDs (MESH:D008107), hepatitis B virus (HBV)/hepatitis C virus (HCV) infection (MESH:D006525), ALD (MESH:D008108)
- **Chemicals:** bile acid (MESH:D001647)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12892347/full.md

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Source: https://tomesphere.com/paper/PMC12892347