Evidence map›Paper›PMID 32760208›Full record

ReviewInternational journal of biological sciences2020

Interleukin 22 in Liver Injury, Inflammation and Cancer.

Ye Wu, Jie Min, Chang Ge, Jinping Shu, Di Tian, Yuan Yuan, Dian Zhou

Open access · goldAbstract readReview
In one paragraph

Review in International journal of biological sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Review
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  18. IL-22/IL-22R1 pathway enhances cholangiocarcinoma progressionWorld journal of gastrointestinal oncology · 2025
    Article
  19. Novel treatment of acute and acute-on-chronic liver failure: Interleukin-22.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  20. Article
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

7 authors at 2 institutions in 1 country.

Ye WuThe First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China.
Jie MinThe Second Hospital of Anhui Medical University, Hefei, Anhui, 230601, China.
Chang GeThe First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui, 230022, China.
Jinping ShuThe First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China.
Di TianThe First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China.
Yuan YuanThe First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China.
Dian ZhouThe First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China.
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 22(IL-22), a member of the IL-10 cytokine family and is an emerging CD4+Th cytokine that plays an important role in anti-microbial defense, homeostasis and tissue repair. We are interested in IL-22 as it has the double function of suppressing or encouraging inflammation in various disease models including hepatic inflammation. As a survival factor for hepatocytes, IL-22 plays a protective role in many kinds of liver diseases, such as hepatitis, liver fibrosis, or hepatocellular carcinoma (HCC) by binding to the receptors IL-22R1 and IL-10R2. Overexpression of IL-22 reduces liver fibrosis by attenuating the activation of hepatic stellate cell (the main cell types involved in hepatic fibrosis), and down-regulating the levels of inflammatory cytokines. Administration of exogenous IL-22 increases the replication of hepatocytes by inhibiting cell apoptosis and promoting mitosis, ultimately plays a contributing role in liver regeneration. Furthermore, treatment with IL-22 activates hepatic signal transducer and activator of transcription 3 (STAT3), ameliorates hepatic oxidative stress and alcoholic fatty liver, effectively alleviate the liver damage caused by alcohol and toxicant. In conclusion, the hepatoprotective functions and liver regeneration promoting effect of IL-22 suggests the therapeutic potential of IL-22 in the treatment of human hepatic diseases.

Indexed as

AnimalsGene Expression RegulationHumansInflammationInterleukin-22InterleukinsLiverNeoplasmsInterleukin-22InterleukinsHCCIL-22InflammationLiver injuryLiver regeneration.

Identifiers

PMID32760208
PMCPMC7378634
OpenAlexW3040671986

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.