Evidence map›Paper›PMID 41235399›Full record

ReviewMedComm2025

The Gut‒Liver Axis in Liver Disease: Molecular Mechanisms and Therapeutic Targets.

Zhiji Chen, Siqi Liao, Suhua Wu, Siyuan Chen, Qin Tang, Li Zhou, Xiaoqin Li, Huiyi Hu, Jiayao Xu, An Zhang and 2 more

Abstract readReview
In one paragraph

Review in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Epistemic compression in large language model explanations of the gut-liver axis.Frontiers in cellular and infection microbiology · 2026
    Article
  7. Article
  8. Review
  9. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Zhiji ChenDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Siqi LiaoDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Suhua WuDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Siyuan ChenDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Qin TangDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Li ZhouDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Xiaoqin LiDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Huiyi HuDepartment of Critical Care Medicine The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Jiayao XuDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
An ZhangDepartment of Critical Care Medicine The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Song HeDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.
Zhi-Hang ZhouDepartment of Gastroenterology The Second Affiliated Hospital of Chongqing Medical University Chongqing China.ORCID https://orcid.org/0000-0003-1356-9872

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increasing global burden of liver disease is a growing public health challenge. The gut‒liver axis, a bidirectional communication system between the intestine and liver via the portal circulation and biliary tract, is crucial for maintaining metabolic and immune homeostasis. Dysregulation of the gut‒liver axis has been recognized as a key driver of the pathogenesis of various liver diseases. However, its complex molecular mechanisms and the resulting precision therapeutic strategies remain under investigation. This review elaborates on the core components of the gut‒liver axis and the key mechanisms of gut‒liver axis imbalance in metabolic dysfunction-associated fatty liver disease, alcohol-associated liver disease, cirrhosis, spontaneous bacterial peritonitis, and primary liver cancer. We discuss the core roles of intestinal barrier dysfunction, dysbiosis, liver immune activation, and bacterial metabolite imbalance. Furthermore, we systematically review emerging therapeutic strategies targeting this axis, such as restoring barrier function, correcting dysbiosis, regulating bacterial metabolism, and blocking deleterious signaling. This review provides an integrative perspective on the pathophysiology of liver diseases and highlights the great potential of targeting the gut‒liver axis in translational medicine to improve the treatment paradigm for liver diseases.

Indexed as

dysbiosisgut–liver axisintestinal barrier dysfunctionliver diseasepathogenesis

Identifiers

PMID41235399
PMCPMC12606024

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.