Evidence map›Paper›PMID 32637060›Full record

ArticleTherapeutic advances in chronic disease2020

Integrin alpha-5 silencing leads to myofibroblastic differentiation in IPF-derived human lung fibroblasts.

Gali Epstein Shochet, Elizabetha Brook, Becky Bardenstein-Wald, Hanna Grobe, Evgeny Edelstein, Lilach Israeli-Shani, David Shitrit

Open access · goldAbstract read
In one paragraph

Article in Therapeutic advances in chronic disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Integrin Alpha8 Beta1 (81): An In-Depth Review of an Overlooked RGD-Binding Receptor.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2025
    Article
  10. Integrins as Drug Targets in Vascular and Related Diseases.International journal of drug discovery and pharmacology · 2024
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Efficacy of Qingfei oral liquid for idiopathic pulmonary fibrosis in rats and related network pharmacology study.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Article
  16. Article
  17. 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

7 authors at 1 institution in 1 country.

Gali Epstein ShochetPulmonary Medicine Department, Meir Medical Department, 59 Tchernichovsky St., Kfar Saba 44281, Israel Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.ORCID https://orcid.org/0000-0002-3417-9171
Elizabetha BrookSackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Becky Bardenstein-WaldSackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Hanna GrobeSackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Evgeny EdelsteinSackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel Pathology Department, Meir Medical Center, Kfar Saba, Israel.
Lilach Israeli-ShaniPulmonary Department, Meir Medical Center, Kfar Saba, Israel Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
David ShitritPulmonary Department, Meir Medical Center, Kfar Saba, Israel Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveThe term 'fibroblast' covers a heterogeneous cell population in idiopathic pulmonary fibrosis (IPF). The fibroblasts are considered as main effector cells, because they promote disease progression by releasing exaggerated amounts of extracellular matrix proteins and modifying cell microenvironment. As IPF-derived human lung fibroblasts (IPF-HLFs) were shown to express higher levels of integrin alpha-5 (ITGA5) than normal derived HLFs (N-HLFs), we explored the importance of ITGA5 to IPF progression.

methodsIPF-HLF and N-HLF primary cultures were established. ITGA5 was silenced by specific small interfering RNA (siRNA)s and its effects on cell phenotype (e.g. cell number, size, cell death, migration) and gene expression (e.g. RNA sequencing, quantitative polymerase chain reaction [qPCR], western blot and immunofluorescence) were tested. Specific integrin expression was evaluated in IPF patient formalin-fixed paraffin embedded sections by immunohistochemistry (IHC).

resultsITGA5-silencing resulted in reduced IPF-HLF proliferation rates and cell migration (

conclusionsITGA5 expression facilitates a more aggressive proliferative phenotype. Downregulation of this integrin results in myofibroblastic differentiation, which is accompanied by elevated ITGA8. Specific targeting could present a therapeutic benefit.

Indexed as

fibroblastsidiopathic pulmonary fibrosisintegrin α5integrin α8siRNA

Identifiers

PMID32637060
PMCPMC7315658
OpenAlexW3038051561

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.