Evidence map›Paper›PMID 34122138›Full record

ReviewFrontiers in physiology2021

Animal and Organoid Models of Liver Fibrosis.

Yu-Long Bao, Li Wang, Hai-Ting Pan, Tai-Ran Zhang, Ya-Hong Chen, Shan-Jing Xu, Xin-Li Mao, Shao-Wei Li

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 1% of its field
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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Combining sorafenib andIranian journal of basic medical sciences · 2026
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  8. Integrating mechanical cues inFrontiers in immunology · 2026
    Review
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  11. Article
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  20. Article

1 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 1 country.

Yu-Long BaoCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Li WangCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Hai-Ting PanCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Tai-Ran ZhangCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Ya-Hong ChenHealth Management Center, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, China.
Shan-Jing XuSchool of Medicine, Shaoxing University, Shaoxing, Chian.
Xin-Li MaoSchool of Medicine, Shaoxing University, Shaoxing, Chian.
Shao-Wei LiKey Laboratory of Minimally Invasive Techniques & Rapid Rehabilitation of Digestive System Tumor, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, China.
Inner Mongolia Medical University · CNWenzhou Medical University · CNShaoxing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis refers to the process underlying the development of chronic liver diseases, wherein liver cells are repeatedly destroyed and regenerated, which leads to an excessive deposition and abnormal distribution of the extracellular matrix such as collagen, glycoprotein and proteoglycan in the liver. Liver fibrosis thus constitutes the pathological repair response of the liver to chronic injury. Hepatic fibrosis is a key step in the progression of chronic liver disease to cirrhosis and an important factor affecting the prognosis of chronic liver disease. Further development of liver fibrosis may lead to structural disorders of the liver, nodular regeneration of hepatocytes and the formation of cirrhosis. Hepatic fibrosis is histologically reversible if treated aggressively during this period, but when fibrosis progresses to the stage of cirrhosis, reversal is very difficult, resulting in a poor prognosis. There are many causes of liver fibrosis, including liver injury caused by drugs, viral hepatitis, alcoholic liver, fatty liver and autoimmune disease. The mechanism underlying hepatic fibrosis differs among etiologies. The establishment of an appropriate animal model of liver fibrosis is not only an important basis for the in-depth study of the pathogenesis of liver fibrosis but also an important means for clinical experts to select drugs for the prevention and treatment of liver fibrosis. The present study focused on the modeling methods and fibrosis characteristics of different animal models of liver fibrosis, such as a chemical-induced liver fibrosis model, autoimmune liver fibrosis model, cholestatic liver fibrosis model, alcoholic liver fibrosis model and non-alcoholic liver fibrosis model. In addition, we also summarize the research and application prospects concerning new organoids in liver fibrosis models proposed in recent years. A suitable animal model of liver fibrosis and organoid fibrosis model that closely resemble the physiological state of the human body will provide bases for the in-depth study of the pathogenesis of liver fibrosis and the development of therapeutic drugs.

Indexed as

animalfibrosislivermodelorganoid

Identifiers

PMID34122138
PMCPMC8187919
OpenAlexW3164973461

What OpenQuestion 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 OpenQuestion graph.