Evidence map›Paper›PMID 39995661›Full record

ReviewFrontiers in immunology2025

The role of the interleukin family in liver fibrosis.

Zixin Zhang, Jiahui Wang, Hui Li, Qun Niu, Yujing Tao, Xin Zhao, Zijian Zeng, Haijian Dong

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–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

26 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Discriminative Role of Interleukin-6, Neuropilin-1, and Amphiregulin for Cirrhosis in Patients with Chronic Hepatitis B Infection.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026
    Article
  5. Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Observational
  19. Article
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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

8 authors.

Zixin ZhangCentral Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Jiahui WangSchool of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Hui LiCentral Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Qun NiuCentral Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Yujing TaoCentral Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Xin ZhaoCentral Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Zijian ZengCentral Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Haijian DongCentral Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis represents a wound-healing response to chronic liver injury caused by viral infections, alcohol, and chemicals agents. It is a critical step in the progression from chronic liver disease to cirrhosis and hepatocellular carcinoma. No chemical or biological drugs have been approved for the treatment of liver fibrosis. Relevant studies have demonstrated that effective inhibition of hepatitis B virus (HBV) replication by nucleoside (acid) analogs or polyethylene glycol alpha-interferon can lead to recovery in some patients with hepatitis B liver fibrosis, However, some patients with liver fibrosis do not show improvement, even after achieving a complete serologic and virologic response. A similar situation occurs in patients with hepatitis C-related liver fibrosis. The liver, with its unique anatomical and immunological structure, is the largest immune organ and produces a large number of cytokines in response to external stimuli, which are crucial for the progression of liver fibrosis. cytokines can act either by directly affecting hepatic stellate cells (HSCs) or by indirectly regulating immune target cells. Among these, the interleukin family activates a complex cascade of responses, including cytokines, chemokines, adhesion molecules, and lipid mediators, playing a key role in the initiation and regulation of inflammation, as well as innate and adaptive immunity. In this paper, we systematically summarize recent literature to elucidate the pathogenesis of interleukin-mediated liver fibrosis and explore potential therapeutic targets for liver fibrosis treatment.

Indexed as

InterleukinsLiver CirrhosisAnimalsHepatic Stellate CellsHumansLiverInterleukinscytokinesinflammationinterleukin receptorsinterleukinsliver fibrosis

Identifiers

PMID39995661
PMCPMC11847652

What OpenQuestion holds

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Registered trials

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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.