Evidence map›Paper›PMID 25388426›Full record

ArticleLiver international : official journal of the International Association for the Study of the Liver2015

Mechanisms of fibrosis in acute liver failure.

Yingli He, Li Jin, Jing Wang, Zhi Yan, Tianyan Chen, Yingren Zhao

Open access · hybridAbstract read
In one paragraph

Article in Liver international : official journal of the International Association for the Study of the Liver, 2015. 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
1.9field-weighted citation impact, top 16% 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, 49 citations in OpenAlex.

  1. Article
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  3. Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026
    Review
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  13. Review
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  15. Article
  16. Autophagy in liver diseases.World journal of hepatology · 2021
    Review
  17. Article
  18. Article
  19. Circular RNA CREBBP Suppresses Hepatic FibrosisFrontiers in pharmacology · 2021
    Article
  20. [Autophagy in the liver failure].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020
    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

6 authors at 2 institutions in 1 country.

Yingli HeDepartment of Infectious Diseases, First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Li JinInstitution of Hepatology, First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi province, China.
Jing WangInstitution of Hepatology, First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi province, China.
Zhi YanInstitution of Hepatology, First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi province, China.
Tianyan ChenDepartment of Infectious Diseases, First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Yingren ZhaoDepartment of Infectious Diseases, First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
First Affiliated Hospital of Xi'an Jiaotong University · CNSecond Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsAcute liver failure (ALF) is a condition with high mortality and morbidity. Fibrosis in chronic liver disease was extensively researched, whereas fibrosis and underlying mechanism in acute liver failure remains unclear.

methodsHepatitis B virus related ALF patients were recruited to investigate if there was ongoing fibrosis by liver histology and liver stiffness measurement(LSM) analysis as well as fibrosis markers assay. Sera HMGB1 were kinetically detected in progression and remission stage of ALF. Hepatic stellate cell(HSC) activation by HMGB1 was explored by testing mRNA and protein level of α-SMA and collagen 1a1 by using qPCR and western blot. Autophagy induction by HMGB1 was explored by LC3-II conversion, autophagy flux and fluorescence.

resultsFirstly, ongoing fibrosis in progression stage of ALF was confirmed by histological analysis, LS measurement as well as fibrosis markers detection. HSC activation and autophagy induction in explanted liver tissue also revealed. Next, kinetic monitoring sera HMGB1 revealed elevated HMGB1 in progression stage of ALF vs HBsAg carrier, and drop back to base level in remission stage. Thirdly, rHMGB1 dose dependently activated HSCs, as indicated by increased mRNA and proteins level in α-SMA and collagen 1a1. Moreover, autophagy was induced in HSC treated with rHMGB1, as illustrated by increased LC3 lipidation, elevated autophagy flux and GFP-LC3 puncta.

conclusionsAcute liver failure is accompanied by ongoing fibrosis, HSC activation and autophagy induction. Increased HMGB1 activates HSC via autophagy induction. Those findings integrate HMGB1, HSCs activation, autophagy into a common framework that underlies the fibrosis in ALF.

Indexed as

ActinsAnimalsAutophagyBiomarkersBiopsyCells, CulturedCollagen Type ICollagen Type I, alpha 1 ChainDisease ProgressionElasticity Imaging TechniquesHepatic Stellate CellsHepatitis BHMGB1 ProteinHumansLiverLiver CirrhosisACTA2 protein, humanActa2 protein, ratActinsAnxa3 protein, ratBiomarkersCollagen Type ICollagen Type I, alpha 1 ChainHMGB1 ProteinHMGB1 protein, humanMAP1LC3A protein, humanMicrotubule-Associated Proteinsacute liver failureautophagyfibrosishepatic stellate cellhepatitis B virushigh mobility group box 1

Identifiers

PMID25388426
PMCPMC5024020
OpenAlexW2091283163

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.