Evidence map›Paper›PMID 27468691›Full record

ArticleCell death & disease2016

Egg antigen p40 of Schistosoma japonicum promotes senescence in activated hepatic stellate cells by activation of the STAT3/p53/p21 pathway.

Jinling Chen, Tianhua Xu, Dandan Zhu, Jianxin Wang, Caiqun Huang, Lei Lyu, Bin Hu, Wei Sun, Yinong Duan

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. rSjP40 Inhibited the Activity of Collagen Type I PromoterFrontiers in cell and developmental biology · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 at 1 institution in 1 country.

Jinling ChenDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Tianhua XuDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Dandan ZhuDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Jianxin WangLaboratory Medicine Center, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Caiqun HuangDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Lei LyuDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Bin HuDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Wei SunDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Yinong DuanDepartment of Pathogen Biology, School of Medicine, Nantong University, Nantong, Jiangsu 226001, People's Republic of China.
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is a serious disease that is characterized by the excess deposition of extracellular matrix (ECM) components. Activated hepatic stellate cells (HSCs) are a major source of ECM and serve as a key regulator in liver fibrogenesis. Inactivation of HSCs is essential for liver fibrotic regression. The present study explores the underlying mechanisms of Schistosoma japonicum egg antigen p40 (Sjp40) promoting senescence in HSCs and antifibrosis. For the first time we report that Sjp40 inhibits the activation and proliferation of an immortalized human HSC line (LX-2 cells) and promotes cellular senescence and cell cycle arrest. Sjp40 through action on the STAT3/p53/p21 pathway triggered cellular senescence, while knockdown of p53 or STAT3 partly restored cell senescence. In addition, Sjp40-induced cellular senescence caused LX-2 cells to be more sensitive to a human NK cell line (YT cells). Together these findings provide novel insights into the mechanism of antifibrosis and may have implications for the development of antifibrosis therapies.

Indexed as

Cellular SenescenceSignal TransductionActinsAnimalsAntigens, HelminthCell LineCell ProliferationCollagen Type ICyclin-Dependent Kinase Inhibitor p21Down-RegulationHelminth ProteinsHepatic Stellate CellsKiller Cells, NaturalPhenotypeSchistosoma japonicumSTAT3 Transcription FactorActinsAntigens, HelminthCollagen Type ICyclin-Dependent Kinase Inhibitor p21Helminth Proteinsp40 egg antigen, SchistosomaSTAT3 Transcription FactorToll-Like Receptor 4Tumor Suppressor Protein p53

Identifiers

PMID27468691
PMCPMC4973363
OpenAlexW2480717462

What OpenQuestion holds

Textmetadata
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.