Evidence map›Paper›PMID 33177520›Full record

ArticleCell death & disease2020

IL-22 ameliorates LPS-induced acute liver injury by autophagy activation through ATF4-ATG7 signaling.

Lujing Shao, Xi Xiong, Yucai Zhang, Huijie Miao, Yuqian Ren, Xiaomeng Tang, Jia Song, Chunxia Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
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  7. Observational
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    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 at 1 institution in 1 country.

Lujing ShaoDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Xi XiongDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Yucai ZhangDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China. zyucai2018@163.com.ORCID 0000-0002-4905-3600
Huijie MiaoDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Yuqian RenDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Xiaomeng TangDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Jia SongDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Chunxia WangDepartment of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China. karencx0465@163.com.ORCID 0000-0003-4550-5208
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uncontrollable inflammatory response acts as a driver of sepsis-associated liver injury (SALI). IL-22 plays an important role in regulating inflammatory responses, but its role in SALI remains unknown. The aim of the study was to assess the association of serum IL-22 with SALI in pediatric patients and to enclose the underlying mechanisms of IL-22 involved in lipopolysaccharide (LPS) - induced acute liver injury (ALI) in mice. Serum IL-22 levels in patients with SALI were significantly lower than in septic patients without liver injury, and the area under receiver operating characteristic (ROC) curve of IL-22 for discriminating SALI was 0.765 (95% CI: 0.593-0.937). Pre-administration of recombinant murine IL-22 alleviated LPS-induced ALI in mice, and serum IL-6 levels and the mRNA levels of TNF-α, IL-1β, and IL-6 in livers were decreased in response to IL-22 pre-treatment in mice. More importantly, IL-22 pre-treatment activated hepatic autophagy mediated by activating transcription factor 4 (ATF4)-autophagy-related gene 7 (ATG7) signaling in vivo and in vitro in response to LPS administration. Moreover, knockdown of ATF4 in mice aggravated LPS-induced ALI, which was associated with suppressed ATG7-related autophagy. In addition, the protective effects of IL-22 on LPS-induced ALI was partially blocked by ATF4 knockdown, which was associated with lower expression of LC3II/I in the livers of ATF4 knockdown (HT or Atf4

Indexed as

Activating Transcription Factor 4Acute Lung InjuryAnimalsAutophagyAutophagy-Related Protein 7HumansInterleukin-22InterleukinsLipopolysaccharidesMaleMiceMice, Inbred C57BLRecombinant ProteinsSignal TransductionActivating Transcription Factor 4Autophagy-Related Protein 7Interleukin-22InterleukinsLipopolysaccharidesRecombinant Proteins

Identifiers

PMID33177520
PMCPMC7658242
OpenAlexW3099745259

What OpenQuestion holds

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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.