Evidence map›Paper›PMID 27010852›Full record

ArticleCell death & disease2016

Inhibition of glycogen synthase kinase 3β promotes autophagy to protect mice from acute liver failure mediated by peroxisome proliferator-activated receptor α.

F Ren, L Zhang, X Zhang, H Shi, T Wen, L Bai, S Zheng, Y Chen, D Chen, L Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Targeting autophagy for combating chemoresistance and radioresistance in glioblastoma.Apoptosis : an international journal on programmed cell death · 2018
    Pooled it
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  15. Targeting the Wnt Signaling Pathway in Liver Fibrosis for Drug Options: An Update.Journal of clinical and translational hepatology · 2021
    Review
  16. Article
  17. Article
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  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

11 authors at 3 institutions in 1 country.

F RenBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
L ZhangBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
X ZhangBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
H ShiBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
T WenBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
L BaiBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
S ZhengBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
Y ChenBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
D ChenBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
L LiDepartment of Cell Biology, Municipal Laboratory for Liver Protection and Regulation of Regeneration, Capital Medical University, Beijing, China.
Z DuanBeijing Artificial Liver Treatment & Training Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China.
Beijing YouAn Hospital · CNCapital Medical University · CNThird Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous studies have demonstrated that inhibition of glycogen synthase kinase 3β (GSK3β) activity protects mice from acute liver failure (ALF), whereas its protective and regulatory mechanism remains elusive. Autophagy is a recently recognized rudimentary cellular response to inflammation and injury. The aim of the present study was to test the hypothesis that inhibition of GSK3β mediates autophagy to inhibit liver inflammation and protect against ALF. In ALF mice model induced by D-galactosamine (D-GalN) and lipopolysaccharide (LPS), autophagy was repressed compared with normal control, and D-GalN/LPS can directly induce autophagic flux in the progression of ALF mice. Autophagy activation by rapamycin protected against liver injury and its inhibition by 3-methyladenine (3-MA) or autophagy gene 7 (Atg7) small interfering RNA (siRNA) exacerbated liver injury. The protective effect of GSK3β inhibition on ALF mice model depending on the induction of autophagy, because that inhibition of GSK3β promoted autophagy in vitro and in vivo, and inhibition of autophagy reversed liver protection and inflammation of GSK3β inhibition. Furthermore, inhibition of GSK3β increased the expression of peroxisome proliferator-activated receptor α (PPARα), and the downregulated PPARα by siRNA decreased autophagy induced by GSK3β inhibition. More importantly, the expressions of autophagy-related gene and PPARα are significantly downregulated and the activity of GSK3β is significantly upregulated in liver of ALF patients with hepatitis B virus. Thus, we have demonstrated the new pathological mechanism of ALF that the increased GSK3β activity suppresses autophagy to promote the occurrence and development of ALF by inhibiting PPARα pathway.

Indexed as

AutophagySignal TransductionAnimalsGalactosamineGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansIsoenzymesLipopolysaccharidesLiver Failure, AcuteMicePPAR alphaSirolimusGalactosamineGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaIsoenzymesLipopolysaccharidesPPAR alphaSirolimus

Identifiers

PMID27010852
PMCPMC4823957
OpenAlexW2304588727

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.