Evidence map›Paper›PMID 33311456›Full record

ArticleCell death & disease2020

Transcriptional factor ATF3 promotes liver fibrosis via activating hepatic stellate cells.

Zhemin Shi, Kun Zhang, Ting Chen, Yu Zhang, Xiaoxiao Du, Yanmian Zhao, Shuai Shao, Lina Zheng, Tao Han, Wei Hong

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
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  4. iScience · 2026
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  9. Review
  10. ATF3 aggravates kidney fibrosis via HDAC6-dependent epigenetic reprogramming.International journal of biological sciences · 2026
    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

10 authors at 2 institutions in 1 country.

Zhemin ShiDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Kun ZhangDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.ORCID 0000-0002-8916-556X
Ting ChenDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yu ZhangDepartment of Hepatology and Gastroenterology, The Third Central Clinical College of Tianjin Medical University, Tianjin, China.
Xiaoxiao DuDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yanmian ZhaoDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Shuai ShaoDepartment of Hepatology and Gastroenterology, Tianjin Third Central Hospital Affiliated to Nankai University, Tianjin, China.
Lina ZhengDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Tao HanDepartment of Hepatology and Gastroenterology, The Third Central Clinical College of Tianjin Medical University, Tianjin, China. hantaomd@126.com.
Wei HongDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China. hongwei@tmu.edu.cn.
Tianjin Medical University · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The excessive accumulation of extracellular matrix (ECM) is a key feature of liver fibrosis and the activated hepatic stellate cells (HSCs) are the major producer of ECM proteins. However, the precise mechanisms and target molecules that are involved in liver fibrosis remain unclear. In this study, we reported that activating transcription factor 3 (ATF3) was over-expressed in mice and human fibrotic livers, in activated HSCs and injured hepatocytes (HCs). Both in vivo and in vitro study have revealed that silencing ATF3 reduced the expression of pro-fibrotic genes and inhibited the activation of HSCs, thus alleviating the extent of liver fibrosis, indicating a potential protective role of ATF3 knockdown. However, ATF3 was not involved in either the apoptosis or proliferation of HCs. In addition, our data illustrated that increased nuclear localization of ATF3 promoted the transcription of fibrogenic genes and lnc-SCARNA10, which functioned as a novel positive regulator of TGF-β signaling in liver fibrogenesis by recruiting SMAD3 to the promoter of these genes. Interestingly, further study also demonstrated that lnc-SCARNA10 promoted the expression of ATF3 in a TGF-β/SMAD3-dependent manner, revealing a TGF-β/ATF3/lnc-SCARNA10 axis that contributed to liver fibrosis by activating HSCs. Taken together, our data provide a molecular mechanism implicating induced ATF3 in liver fibrosis, suggesting that ATF3 may represent a useful target in the development of therapeutic strategies for liver fibrosis.

Indexed as

Activating Transcription Factor 3AnimalsCarbon TetrachlorideCells, CulturedFeedback, PhysiologicalGene Expression RegulationHepatic Stellate CellsHumansLiver CirrhosisMiceRNA, Long NoncodingSmad3 ProteinTransforming Growth Factor betaUp-RegulationActivating Transcription Factor 3Carbon TetrachlorideRNA, Long NoncodingSmad3 ProteinTransforming Growth Factor beta

Identifiers

PMID33311456
PMCPMC7734065
OpenAlexW3110665170

What OpenQuestion holds

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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.