Evidence map›Paper›PMID 25892868›Full record

ArticleWorld journal of gastroenterology2015

Early activated hepatic stellate cell-derived molecules reverse acute hepatic injury.

Wen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Fibroblasts in liver cancer: functions and therapeutic translation.The lancet. Gastroenterology & hepatology · 2023
    Review
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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

10 authors at 1 institution in 1 country.

Wen-Ju ChangWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Lu-Jun SongWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Tuo YiWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Kun-Tang ShenWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Hong-Shan WangWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Xiao-Dong GaoWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Min LiWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Jian-Min XuWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Wei-Xin NiuWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Xin-Yu QinWen-Ju Chang, Lu-Jun Song, Tuo Yi, Kun-Tang Shen, Hong-Shan Wang, Xiao-Dong Gao, Min Li, Jian-Min Xu, Wei-Xin Niu, Xin-Yu Qin, Department of General Surgery, Zhongshan Hospital, Institute of General Surgery, Fudan University, Shanghai 200032, China.
Zhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo test whether hepatic stellate cells (HSCs) at different activation stages play different roles in acetaminophen (APAP)-induced acute liver injury (ALI).

methodsHSCs were isolated from mouse liver and cultured in vitro. Morphological changes of initiation HSCs [HSCs (5d)] and perpetuation HSCs [HSCs (p3)] were observed by immunofluorescence and transmission electron microscopy. The protective effects of HSC-derived molecules, cell lysates and HSC-conditioned medium (HSC-CM) were tested in vivo by survival and histopathological analyses. Liver injury was determined by measuring aminotransferase levels in the serum and by histologic examination of tissue sections under a light microscope. Additionally, to determine the molecular mediators of the observed protective effects of initiation HSCs, we examined HSC-CM using a high-density protein array.

resultsHSCs (5d) and HSCs (p3) had different morphological and phenotypic traits. HSCs (5d) presented a star-shaped appearance with expressing α-SMA at non-uniform levels between cells. However, HSCs (p3) evolved into myofibroblast-like cells without lipid droplets and expressed a uniform and higher level of α-SMA. HSC-CM (5d), but not HSC-CM (p3), provided a significant survival benefit and showed a dramatic reduction of hepatocellular necrosis and panlobular leukocyte infiltrates in mice exposed to APAP. However, this protective effect was abrogated at higher cell masses, indicating a therapeutic window of effectiveness. Furthermore, the protein array screen revealed that HSC-CM (5d) was composed of many chemokines and growth factors that correlated with inflammatory inhibition and therapeutic activity. When compared with HSC-CM (p3), higher levels of monocyte chemoattractant protein-1, macrophage inflammatory protein-1γ, hepatocyte growth factor, interleukin-10, and matrix metalloproteinase-2, but lower levels of stem cell factor and Fas-Ligand were observed in HSC-CM (5d).

conclusionThese data indicated that initiation HSCs and perpetuation HSCs were different in morphology and protein expression, and provided the first experimental evidence of the potential medical value of initiation HSC-derived molecules in the treatment of ALI.

Indexed as

Paracrine CommunicationAcetaminophenAnimalsAnti-Inflammatory AgentsCells, CulturedCell ShapeChemical and Drug Induced Liver InjuryChemokinesCulture Media, ConditionedDisease Models, AnimalHepatic Stellate CellsIntercellular Signaling Peptides and ProteinsLiverMaleMice, Inbred C57BLNecrosisAcetaminophenAnti-Inflammatory AgentsChemokinesCulture Media, ConditionedIntercellular Signaling Peptides and ProteinsAcute liver injuryHepatic stellate cellsInitiation and perpetuation

Identifiers

PMID25892868
PMCPMC4394079
OpenAlexW2321202230

What OpenQuestion holds

Textmetadata
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Registered trials

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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.