Evidence map›Paper›PMID 34705621›Full record

ArticleAmerican journal of respiratory cell and molecular biology2022

Asporin Promotes TGF-β-induced Lung Myofibroblast Differentiation by Facilitating Rab11-Dependent Recycling of TβRI.

Shaojie Huang, Xiaofan Lai, Lu Yang, Fang Ye, Chanyan Huang, Yuan Qiu, Sijia Lin, Lvya Pu, Zhongxing Wang, Wenqi Huang

Abstract read
PubMed Publisher
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.5field-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

33 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Shaojie HuangDepartment of Cardiac Surgery and.
Xiaofan LaiDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0002-0898-1654
Lu YangDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Fang YeDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Chanyan HuangDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0002-3155-5127
Yuan QiuCenter for Stem Cell Biology and Tissue Engineering, Key Laboratory for Stem Cells and Tissue Engineering, Sun Yat-sen University, Guangzhou, China; and.
Sijia LinSun Yat-sen University, Guangzhou, China.
Lvya PuSun Yat-sen University, Guangzhou, China.
Zhongxing WangDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Wenqi HuangDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0001-7845-1694
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive fibrotic lung disease with high mortality and morbidity. ASPN (asporin), a member of the small leucine-rich proteoglycan family, plays crucial roles in tissue injury and regeneration. However, the precise pathophysiological role of ASPN and its molecular mechanisms in IPF remain unknown. We sought to investigate the role of ASPN during the development of pulmonary fibrosis and the therapeutic potential of targeting ASPN-related signaling pathways. In our study, three microarray datasets were downloaded from the Gene Expression Omnibus database, and differentially expressed genes were screened out by bioinformatic analysis. Hub genes were selected from the protein-protein interaction network. ASPN was examined in lung tissues from pulmonary fibrosis mouse models, and the role of ASPN in transforming growth factor (TGF)-β/Smad signaling was determined by transfection with ASPN shRNA vectors

Indexed as

AnimalsAntibiotics, AntineoplasticBleomycinCase-Control StudiesDisease Models, AnimalExtracellular Matrix ProteinsGene Expression ProfilingGene Regulatory NetworksHumansLungMiceMice, Inbred C57BLMyofibroblastsProtein Interaction MapsPulmonary Fibrosisrab11 GTP-Binding ProteinsAntibiotics, AntineoplasticAspn protein, mouseBleomycinExtracellular Matrix Proteinsrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsReceptor, Transforming Growth Factor-beta Type ITransforming Growth Factor betaASPNbioinformatic analysisidiopathic pulmonary fibrosisRab11TβRI recycling

Identifiers

PMID34705621
OpenAlexW3209009141

What OpenQuestion holds

Textmetadata
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.