Evidence map›Paper›PMID 29196956›Full record

ArticleDigestive diseases and sciences2018

ASPP2 Inhibits the Profibrotic Effects of Transforming Growth Factor-β1 in Hepatic Stellate Cells by Reducing Autophagy.

Minghua Lin, Yuan Chang, Fang Xie, Ying Shi, Lijun Pang, Dexi Chen

Open access · hybridAbstract read
In one paragraph

Article in Digestive diseases and sciences, 2018. 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
1.0field-weighted citation impact, top 24% 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, 18 citations in OpenAlex.

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  6. Review
  7. [Construction of apoptosis-stimulating of p53 protein 2 gene knockout mice and its effect on diethylnitrosamine-induced liver cancer].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020
    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

6 authors at 2 institutions in 1 country.

Minghua LinBeijing Youan Hospital, Beijing Institute of Hepatology, Capital Medical University, Beijing, 100069, China.
Yuan ChangBeijing Youan Hospital, Beijing Institute of Hepatology, Capital Medical University, Beijing, 100069, China.
Fang XieBeijing Youan Hospital, Beijing Institute of Hepatology, Capital Medical University, Beijing, 100069, China.
Ying ShiBeijing Youan Hospital, Beijing Institute of Hepatology, Capital Medical University, Beijing, 100069, China.
Lijun PangBeijing Youan Hospital, Beijing Institute of Hepatology, Capital Medical University, Beijing, 100069, China.
Dexi ChenBeijing Youan Hospital, Beijing Institute of Hepatology, Capital Medical University, Beijing, 100069, China. dexichen@ccmu.edu.cn.
Capital Medical University · CNBeijing YouAn Hospital · CN

Funding

Basics-Clinical Research Cooperation Fund of Capital Medical University,China 15JL-L05Beijing Municipal Institute of Public Medical Research Development and Reform Pilot Project (JING YI YAN 2016-2)the National Natural and Science Foundation of China 81672026
6 · The paper itself

Abstract

backgroundApoptosis-stimulating protein of p53-2 (ASPP2) is a damage-inducible P53-binding protein that enhances damage-induced apoptosis. Fibrosis is a wound-healing response, and hepatic stellate cells (HSCs) are key players in liver fibrogenesis. However, little is known about the relationship between ASPP2 and hepatic fibrosis.

aimsWe investigated the effects of ASPP2 overexpression in HSCs and the role of ASPP2 in mouse liver fibrogenesis.

methodsHuman HSCs (LX-2 cells) were pre-incubated with GFP adenovirus (Ad) or ASPP2 adenovirus (AdASPP2) for 24 h and then treated with or without TGF-β1. ASPP2

resultsIn this study, ASPP2 was found to markedly inhibit TGF-β1-induced fibrogenic activation of LX-2 cells. Further experiments using an autophagic flux assay confirmed that ASPP2 reduced the fibrogenic activation of LX-2 cells by inhibiting autophagy. Moreover, we found that ASPP2 overexpression attenuated the anti-apoptotic effects of TGF-β1 in LX-2 cells. The extent of liver fibrosis was markedly reduced in ASPP2+/+ mouse liver tissue compared with control mice; however, in ASPP2

conclusionThese results suggest that TGF-β1-induced autophagy is required for the fibrogenic response in LX-2 cells and that ASPP2 may both inhibit TGF-β1-induced autophagy and decrease liver fibrosis.

Indexed as

AnimalsApoptosis Regulatory ProteinsAutophagyCarbon Tetrachloride PoisoningCell LineGene Expression RegulationHepatic Stellate CellsHumansLiver CirrhosisMiceMice, Inbred BALB CTransforming Growth Factor beta1Tumor Suppressor ProteinsApoptosis Regulatory ProteinsTP53BP2 protein, humanTransforming Growth Factor beta1Trp53bp2 protein, mouseTumor Suppressor ProteinsASPP2AutophagyHepatic stellate cellTransforming growth factor-β1

Identifiers

PMID29196956
PMCPMC5760593
OpenAlexW2774861550

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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.