Evidence map›Paper›PMID 35659360›Full record

ArticleStem cell research & therapy2022

Human amniotic mesenchymal stem cells-derived IGFBP-3, DKK-3, and DKK-1 attenuate liver fibrosis through inhibiting hepatic stellate cell activation by blocking Wnt/β-catenin signaling pathway in mice.

Quan-Wen Liu, Yan-Min Ying, Jia-Xin Zhou, Wen-Jie Zhang, Zhao-Xiao Liu, Bing-Bing Jia, Hao-Cheng Gu, Chu-Yu Zhao, Xiao-Hui Guan, Ke-Yu Deng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 57 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Quan-Wen LiuThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China.
Yan-Min YingThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China.
Jia-Xin ZhouThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China.
Wen-Jie ZhangThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China.
Zhao-Xiao LiuDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, People's Republic of China.
Bing-Bing JiaZhejiang Provincial Key Lab of Geriatrics, Department of Geriatrics, Zhejiang Hospital, Hangzhou, 310013, People's Republic of China.
Hao-Cheng GuThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China.
Chu-Yu ZhaoThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China.
Xiao-Hui GuanThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China.
Ke-Yu DengThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China. dky@ncu.edu.cn.
Hong-Bo XinThe National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Nanchang University, No. 1299 Xuefu Road, Honggutan District, Nanchang, 330031, Jiangxi Province, People's Republic of China. xinhb@ncu.edu.cn.ORCID 0000-0002-2143-5092
Nanchang University · CNZhejiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLiver fibrosis is an outcome of restoring process in chronic liver injury. Human amniotic mesenchymal stem cells (hAMSCs) derived from amniotic membrane have multilineage differentiation, immunosuppressive, and anti-inflammatory potential which makes them suitable for treating liver fibrosis. This study aimed to explore the effect and mechanism of hAMSCs on liver fibrosis.

methodshAMSCs were transplanted into carbon tetrachloride (CCl

resultsOur results showed that hAMSCs possessed the characterizations of mesenchymal stem cells. hAMSCs significantly reduced liver fibrosis and improved liver function in mice by inhibiting HSCs activation in vivo. Both hAMSCs and hAMSC-CM remarkably inhibited the collagen deposition and activation of LX-2 cells in vitro. Antibody array assay showed that insulin-like growth factor binding protein-3 (IGFBP-3), Dickkopf-3 (DKK-3), and Dickkopf-1 (DKK-1) were highly expressed in the co-culture group and hAMSC-CM group compared with LX-2 group. Western blot assay demonstrated that IGFBP-3, DKK-3, and DKK-1 derived from hAMSCs inhibit LX-2 cell activation through blocking canonical Wnt signaling pathway.

conclusionsOur results demonstrated that IGFBP-3, Dkk3, and DKK-1 secreted by hAMSCs attenuated liver fibrosis in mice through inhibiting HSCs activation via depression of Wnt/β-catenin signaling pathway, suggesting that hAMSCs or hAMSC-CM provides an alternative therapeutic approach for the treatment of liver fibrosis.

Indexed as

Mesenchymal Stem CellsWnt Signaling PathwayAmnionAnimalsHepatic Stellate CellsHumansInsulin-Like Growth Factor Binding Protein 3Liver CirrhosisMicePhosphatidylinositol 3-KinasesInsulin-Like Growth Factor Binding Protein 3Phosphatidylinositol 3-KinasesAntibody arrayHepatic stellate cellHuman amniotic mesenchymal stem cellsLiver fibrosisWnt/β-catenin signaling pathway

Identifiers

PMID35659360
PMCPMC9166579
OpenAlexW4281763942

What OpenQuestion holds

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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.