Evidence map›Paper›PMID 42772945›Full record

ArticleBMJ open gastroenterology2026

Tong Liu, Mengru Wang, Guoliang Zheng, Yuying Wu, Jiankun Shen, Xueqing Dong, Qikai Sun, Yanfei Zhang, Wenfang Tian

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMJ open gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Tong Liu *Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, School of Pharmacy, Hefei, China.
Mengru Wang *Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, School of Pharmacy, Hefei, China.
Guoliang ZhengInflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, School of Pharmacy, Hefei, China.
Yuying WuInflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, School of Pharmacy, Hefei, China.
Jiankun ShenInflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, School of Pharmacy, Hefei, China.
Xueqing DongInflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, School of Pharmacy, Hefei, China.
Qikai SunDepartment of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, China tianwenfang@ahmu.edu.cn yfy1032751@fy.ahmu.edu.cn zyf@ahyz.edu.cn.ORCID http://orcid.org/0000-0002-9733-1943
Yanfei ZhangDepartment of Basic Medicine, Anhui Institute of Medicine, Hefei, China tianwenfang@ahmu.edu.cn yfy1032751@fy.ahmu.edu.cn zyf@ahyz.edu.cn.ORCID http://orcid.org/0009-0000-9298-3339
Wenfang TianInflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, School of Pharmacy, Hefei, China tianwenfang@ahmu.edu.cn yfy1032751@fy.ahmu.edu.cn zyf@ahyz.edu.cn.ORCID http://orcid.org/0000-0001-8285-7531

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveLiver fibrosis is characterised by excessive accumulation of extracellular matrix and can ultimately progress to cirrhosis and malignant transformation. Activation of hepatic stellate cells (HSCs), largely driven by transforming growth factor-beta (TGF-β) signalling, is a central event in fibrogenesis. SAE1 is a subunit of the small ubiquitin-like modifier-activating enzyme E1; its role in liver fibrosis and HSC activation remains unclear. This study aimed to investigate the regulatory function and underlying mechanism of SAE1 in hepatic fibrogenesis.

methodsA carbon tetrachloride (CCl

resultsSAE1 expression was significantly increased in fibrotic livers.

conclusionSAE1 contributes to liver fibrosis by maintaining TGF-β receptor stability and enhancing TGF-β/SMAD-driven HSC activation. These results highlight SAE1 as a potential target for antifibrotic therapy.

Indexed as

Liver CirrhosisReceptors, Transforming Growth Factor betaAnimalsCarbon TetrachlorideDisease Models, AnimalGene Knockdown TechniquesHepatic Stellate CellsHumansMaleMiceMice, Inbred C57BLProteasome Endopeptidase ComplexSignal TransductionTransforming Growth Factor betaUbiquitinationCarbon TetrachlorideProteasome Endopeptidase ComplexReceptors, Transforming Growth Factor betaTransforming Growth Factor betaHEPATIC FIBROSISHEPATIC STELLATE CELLLIVER

Identifiers

PMID42772945
PMCPMC13599849

What OpenQuestion holds

Textmetadata
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.