Evidence map›Paper›PMID 30154452›Full record

ArticleCell death & disease2018

Overexpression of homeodomain-interacting protein kinase 2 (HIPK2) attenuates sepsis-mediated liver injury by restoring autophagy.

Zhengyu Jiang, Lulong Bo, Yan Meng, Chen Wang, Tianxing Chen, Changli Wang, Xiya Yu, Xiaoming Deng

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  10. HIPK2 in the physiology of nervous system and its implications in neurological disorders.Biochimica et biophysica acta. Molecular cell research · 2023
    Review
  11. Article
  12. Review
  13. HIPK2 phosphorylates HDAC3 for NF-κB acetylation to ameliorate colitis-associated colorectal carcinoma and sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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 3 institutions in 1 country.

Zhengyu JiangFaculty of Anesthesiology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Lulong BoFaculty of Anesthesiology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Yan MengFaculty of Anesthesiology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Chen WangDepartment of Cell Biology, School of Basic Medicine, Second Military Medical University, Shanghai, 200433, China.
Tianxing ChenSchool of Life Science, Nanjing University, 210023, Nanjing, Jiangsu Province, China.
Changli WangFaculty of Anesthesiology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Xiya YuFaculty of Anesthesiology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China. yuxiyash@163.com.
Xiaoming DengFaculty of Anesthesiology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China. deng_x@yahoo.com.
Second Military Medical University · CNChanghai Hospital · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is the leading cause of death in intensive care units worldwide. Autophagy has recently been shown to protect against sepsis-induced liver injury. Here, we investigated the roles of homeodomain-interacting protein kinase 2 (HIPK2) in the molecular mechanism of sepsis-induced liver injury. HIPK2 expression was reduced in sepsis-induced liver injury, and HIPK2 overexpression increased the survival rate and improved caecal ligation and puncture (CLP)-induced liver injury by reducing serum and liver aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP) levels in mice with sepsis. HIPK2 overexpression significantly decreased CLP-induced release of inflammatory cytokines into the serum and attenuated oxidative stress-associated indicators in mice with CLP-induced liver injury, whereas HIPK2 knockdown produced the opposite results, suggesting that HIPK2 is a negative regulator of sepsis. Furthermore, HIPK2 overexpression inhibited lipopolysaccharide (LPS)-induced apoptosis of primary hepatocytes, increased the autophagic flux, and restored both autophagosome and autolysosome formation in the livers of CLP-induced mice by suppressing calpain signalling. Importantly, HIPK2 overexpression reduced the elevated cytosolic Ca

Indexed as

Alanine TransaminaseAnimalsApoptosisAspartate AminotransferasesAutophagyCarrier ProteinsCytokinesHepatocytesInflammationLiverLiver DiseasesMaleMiceMice, Inbred C57BLProtein Serine-Threonine KinasesSepsisAlanine TransaminaseAspartate AminotransferasesCarrier ProteinsCytokinesHipk2 protein, mouseProtein Serine-Threonine Kinases

Identifiers

PMID30154452
PMCPMC6113252
OpenAlexW2889539638

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.