Evidence map›Paper›PMID 31907348›Full record

ArticleCell death & disease2020

Intracellular XBP1-IL-24 axis dismantles cytotoxic unfolded protein response in the liver.

Jianye Wang, Bian Hu, Zhicong Zhao, Haiyan Zhang, He Zhang, Zhenjun Zhao, Xiong Ma, Bin Shen, Beicheng Sun, Xingxu Huang and 2 more

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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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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

12 authors at 6 institutions in 2 countries.

Jianye WangDepartment of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.ORCID http://orcid.org/0000-0001-9612-8858
Bian HuSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Zhicong ZhaoDepartment of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Haiyan ZhangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
He ZhangDepartment of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Zhenjun ZhaoDepartment of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Xiong MaDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, and Shanghai Institute of Digestive Disease, Shanghai, China.
Bin ShenState Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University, Nanjing, China.ORCID http://orcid.org/0000-0002-8946-8448
Beicheng SunDepartment of Hepatobiliary Surgery, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
Xingxu HuangSchool of Life Science and Technology, ShanghaiTech University, Shanghai, China. huangxx@shanghaitech.edu.cn.
Jiajie HouState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Qiang XiaDepartment of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China. xiaqiang@shsmu.edu.cn.
Renji Hospital · CNSun Yat-sen University · CNShanghaiTech University · CNNanjing Drum Tower Hospital · CNNanjing Medical University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress-associated cell death is prevalent in various liver diseases. However, the determinant mechanism how hepatocytes survive unresolved stress was still unclear. Interleukin-24 (IL-24) was previously found to promote ER stress-mediated cell death, and yet its expression and function in the liver remained elusive. Here we identified an antiapoptotic role of IL-24, which transiently accumulated within ER-stressed hepatocytes in a X-box binding protein 1 (XBP1)-dependent manner. Disruption of IL-24 increased cell death in the CCL

Indexed as

ApoptosisSignal TransductionUnfolded Protein ResponseAnimalseIF-2 KinaseEndoplasmic Reticulum StressEukaryotic Initiation Factor-2HepatocytesHomeostasisInterleukin-24InterleukinsIntracellular SpaceLiverMice, Inbred C57BLModels, BiologicalTranscription Factor CHOPeIF-2 KinaseEukaryotic Initiation Factor-2Interleukin-24InterleukinsTranscription Factor CHOPX-Box Binding Protein 1

Identifiers

PMID31907348
PMCPMC6944701
OpenAlexW2997178569

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.