Evidence map›Paper›PMID 25946003›Full record

ArticlePloS one2015

IL-11 Attenuates Liver Ischemia/Reperfusion Injury (IRI) through STAT3 Signaling Pathway in Mice.

Miao Zhu, Bo Lu, Qinhong Cao, Zhenfeng Wu, Zhe Xu, Weisu Li, Xuequan Yao, Fukun Liu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
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  4. The role of IL-11 in chronic diseases.Frontiers in immunology · 2026
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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 at 2 institutions in 1 country.

Miao ZhuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of TCM, 155 Hanzhong Road, Nanjing, Jiangsu Province, P. R China.
Bo LuDepartment of General Surgery, Yixing People's Hospital, 75 Tongzhenguan Road, Yixing, Jiangsu Province, P. R China.
Qinhong CaoDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of TCM, 155 Hanzhong Road, Nanjing, Jiangsu Province, P. R China.
Zhenfeng WuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of TCM, 155 Hanzhong Road, Nanjing, Jiangsu Province, P. R China.
Zhe XuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of TCM, 155 Hanzhong Road, Nanjing, Jiangsu Province, P. R China.
Weisu LiDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of TCM, 155 Hanzhong Road, Nanjing, Jiangsu Province, P. R China.
Xuequan YaoDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of TCM, 155 Hanzhong Road, Nanjing, Jiangsu Province, P. R China.
Fukun LiuDepartment of Surgical Oncology, Affiliated Hospital of Nanjing University of TCM, 155 Hanzhong Road, Nanjing, Jiangsu Province, P. R China.
Nanjing University · CNJiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe protective role of IL-11, an IL-6 family cytokine, has been implicated in ischemia/reperfusion injury (IRI) in the heart and kidney, but its role has not been elucidated in liver IRI. This study was designed to evaluate the effects of IL-11 and its mechanism of action on liver IRI in a mouse model.

methodsA partial (70%) warm liver IRI was induced by interrupting the artery/portal vein blood supply to the left/middle liver lobes. IL-11 mRNA expression of ischemic liver after reperfusion was analyzed. Signal transducer and activator of transcription 3 (STAT3) was analyzed following IL-11 treatment in vivo and in vitro. Next, IL-11 was injected intraperitoneally (ip) 1 hour before ischemia. Liver injury was assessed based on serum alanine aminotransferase levels and histopathology. Apoptosis and inflammation were also determined in the ischemic liver. To analyze the role of STAT3 in IL-11 treatment, STAT3 siRNA or non-specific (NS) siRNA was used in vitro and in vivo.

resultsIL-11 mRNA expression was significantly increased after reperfusion in the ischemic liver. STAT3, as a target of IL-11, was activated in hepatocytes after IL-11 treatment in vivo and in vitro. Next, effects of IL-11/STAT3 signaling pathway were assessed in liver IRI, which showed IL-11 treatment significantly attenuated liver IRI, as evidenced by reduced hepatocellular function and hepatocellular necrosis/apoptosis. In addition, IL-11 treatment significantly inhibited the gene expressions of pro-inflammatory cytokines (TNF-α and IL-10) and chemokines (IP-10 and MCP-1). To determine the role of STAT3 in the hepatoprotective effects of IL-11, STAT3 siRNA or NS siRNA was used prior to IL-11 treatment. The results showed STAT3 knockdown abrogated the protective effects of IL-11 in vitro and in vivo.

conclusionsThis work provides first-time evidence for the protective effect of IL-11 treatment on hepatocyte in liver IRI, through the activation of the STAT3 pathway.

Indexed as

Alanine TransaminaseAnimalsApoptosisCells, CulturedChemokine CCL2Chemokine CXCL10Enzyme ActivationInflammationInterleukin-10Interleukin-11LiverMaleMiceMice, Inbred C57BLReperfusion InjuryRNA InterferenceAlanine TransaminaseCcl2 protein, mouseChemokine CCL2Chemokine CXCL10Cxcl10 protein, mouseIL10 protein, mouseInterleukin-10Interleukin-11RNA, Small InterferingStat3 protein, mouseSTAT3 Transcription FactorTumor Necrosis Factor-alpha

Identifiers

PMID25946003
PMCPMC4422694
OpenAlexW267567551

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LicenceCC BY
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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.