Evidence map›Paper›PMID 28061452›Full record

ArticleOncotarget2017

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting autophagy in mice.

Hongbo Shi, Weijia Han, Honglin Shi, Feng Ren, Dexi Chen, Yu Chen, Zhongping Duan

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

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  11. Protective Effect ofNutrients · 2021
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  15. [Autophagy in the liver failure].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020
    Article
  16. Article
  17. Article
  18. Mycelium Polysaccharides fromInternational journal of molecular sciences · 2019
    Article
  19. 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

7 authors at 2 institutions in 1 country.

Hongbo ShiBeijing Youan Hospital, Capital Medical University, Beijing, China.
Weijia HanBeijing Youan Hospital, Capital Medical University, Beijing, China.
Honglin ShiBeijing Youan Hospital, Capital Medical University, Beijing, China.
Feng RenBeijing Youan Hospital, Capital Medical University, Beijing, China.
Dexi ChenBeijing Youan Hospital, Capital Medical University, Beijing, China.
Yu ChenBeijing Youan Hospital, Capital Medical University, Beijing, China.
Zhongping DuanBeijing Youan Hospital, Capital Medical University, Beijing, China.
Beijing YouAn Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAugmenter of liver regeneration (ALR) exerts strong hepatoprotective properties in various animal models of liver injury, but its protective mechanisms have not yet been explored. Autophagy is a recently recognized rudimentary cellular response to inflammation and injury. The aim of this study was to test the hypothesis that ALR may protect against acute liver injury through the autophagic pathway.

methodsThe level and role of ALR in liver injury were studied in a mouse model of acute liver injury induced by carbon tetrachloride (CCl4). The effect of ALR on autophagy was analyzed in vitro and in vivo. After autophagy was inhibited by 3-methyladenine (3-MA), apoptosis and proliferation were detected in the mouse model with acute liver injury. The ALR and autophagic levels were measured in patients with liver cirrhosis (LC) and acute liver failure (ALF), respectively.

resultsDuring the progression of acute liver injury, the ALR levels increased slightly in early stage and significantly decreased in late stage in mice. Treatment with an ALR plasmid via tail vein injection protected mice against acute liver injury. The protective effect of ALR relied on the induction of autophagy, which was supported by the following evidence: (1) ALR overexpression directly induced autophagy flux in vitro and in vivo; and (2) ALR treatment suppressed apoptosis and promoted proliferation in mice exposed to CCl4, but the inhibition of autophagy reversed these effects. More importantly, the ALR levels decreased in patients with LC and ALF compared with normal controls.

conclusionWe demonstrated that ALR ameliorated liver injury via an autophagic mechanism, which indicates a potential therapeutic application for liver injury.

Indexed as

AnimalsAutophagyBlotting, WesternCarbon TetrachlorideChemical and Drug Induced Liver InjuryDisease Models, AnimalHumansLiver CirrhosisLiver DiseasesLiver Failure, AcuteMaleMice, Inbred BALB CMicroscopy, Electron, TransmissionMicroscopy, FluorescenceOxidoreductases Acting on Sulfur Group DonorsReal-Time Polymerase Chain ReactionCarbon TetrachlorideGFER protein, mouseOxidoreductases Acting on Sulfur Group Donorsapoptosisaugmenter of liver regenerationautophagyliver injuryPathology Sectionproliferation

Identifiers

PMID28061452
PMCPMC5355041
OpenAlexW2570685249

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.