Evidence map›Paper›PMID 26713258›Full record

ArticlePeerJ2015

Orphan nuclear receptor NR4A2 inhibits hepatic stellate cell proliferation through MAPK pathway in liver fibrosis.

Pengguo Chen, Jie Li, Yan Huo, Jin Lu, Lili Wan, Bin Li, Run Gan, Cheng Guo

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  9. IGF2-NR4A2 Signaling Regulates Macrophage Subtypes to Attenuate Liver Cirrhosis.Journal of clinical and translational hepatology · 2023
    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

8 authors at 2 institutions in 1 country.

Pengguo ChenDepartment of Pharmacy, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China ; Shanghai Jiao Tong University School of Medicine , Shanghai , China.
Jie LiDepartment of Pharmacy, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Yan HuoDepartment of Pharmacy, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Jin LuDepartment of Pharmacy, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Lili WanDepartment of Pharmacy, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Bin LiDepartment of Pharmacy, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Run GanDepartment of Pharmacy, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China.
Cheng GuoDepartment of Pharmacy, Shanghai Jiao Tong University Affiliated Sixth People's Hospital , Shanghai , China ; Shanghai Jiao Tong University School of Medicine , Shanghai , China.
Shanghai Sixth People's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic stellate cells (HSCs) play a crucial role in liver fibrosis, which is a pathological process characterized by extracellular matrix accumulation. NR4A2 is a nuclear receptor belonging to the NR4A subfamily and vital in regulating cell growth, metabolism, inflammation and other biological functions. However, its role in HSCs is unclear. We analyzed NR4A2 expression in fibrotic liver and stimulated HSCs compared with control group and studied the influence on cell proliferation, cell cycle, cell apoptosis and MAPK pathway after NR4A2 knockdown. NR4A2 expression was examined by real-time polymerase chain reaction, Western blotting, immunohistochemistry and immunofluorescence analyses. NR4A2 expression was significantly lower in fibrotic liver tissues and PDGF BB or TGF-β stimulated HSCs compared with control group. After NR4A2 knockdown α-smooth muscle actin and Col1 expression increased. In addition, NR4A2 silencing led to the promotion of cell proliferation, increase of cell percentage in S phase and reduced phosphorylation of ERK1/2, P38 and JNK in HSCs. These results indicate that NR4A2 can inhibit HSC proliferation through MAPK pathway and decrease extracellular matrix in liver fibrogenesis. NR4A2 may be a promising therapeutic target for liver fibrosis.

Indexed as

FibrosisHepatic stellate cellMAPKNR4A2Proliferation

Identifiers

PMID26713258
PMCPMC4690364
OpenAlexW2261617679

What OpenQuestion holds

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LicenceCC BY
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.