Evidence map›Paper›PMID 33805152›Full record

ArticleInternational journal of molecular sciences2021

Hypoxia Inducible Factor 1A Supports a Pro-Fibrotic Phenotype Loop in Idiopathic Pulmonary Fibrosis.

Gali Epstein Shochet, Becky Bardenstein-Wald, Mary McElroy, Andrew Kukuy, Mark Surber, Evgeny Edelstein, Barak Pertzov, Mordechai Reuven Kramer, David Shitrit

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.0field-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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. MCT4 mediates hypoxia-induced extracellular lactate release from IPF fibroblasts.American journal of respiratory cell and molecular biology · 2026
    Article
  3. Article
  4. Article
  5. Immune dysregulation inFrontiers in immunology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Prostaglandin E2 (PGE2) and Roflumilast Involvement in IPF Progression.International journal of molecular sciences · 2023
    Review
  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 4 institutions in 2 countries.

Gali Epstein ShochetPulmonary Department, Meir Medical Center, Kfar Saba 4428164, Israel.
Becky Bardenstein-WaldSackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.
Mary McElroyRespiratory Pharmacology, Charles River Laboratories, Edinburgh EH33 2NE, UK.
Andrew KukuyThe Leviev Heart Institute, Sheba Medical Center, Ramat Gan 5262000, Israel.
Mark SurberAvalyn Pharma, 701 Pike Street suite 1500, Seattle, WA 98101, USA.ORCID 0000-0001-8868-9233
Evgeny EdelsteinPathology Department, Meir Medical Center, Kfar Saba 4428164, Israel.
Barak PertzovSackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.ORCID 0000-0002-3077-3616
Mordechai Reuven KramerSackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.
David ShitritPulmonary Department, Meir Medical Center, Kfar Saba 4428164, Israel.
Tel Aviv University · ILCharles River Laboratories (United Kingdom) · GBMeir Medical Center · ILSheba Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with poor prognosis. The IPF-conditioned matrix (IPF-CM) system enables the study of matrix-fibroblast interplay. While effective at slowing fibrosis, nintedanib has limitations and the mechanism is not fully elucidated. In the current work, we explored the underlying signaling pathways and characterized nintedanib involvement in the IPF-CM fibrotic process. Results were validated using IPF patient samples and bleomycin-treated animals with/without oral and inhaled nintedanib. IPF-derived primary human lung fibroblasts (HLFs) were cultured on Matrigel and then cleared using NH

Indexed as

AnimalsBleomycinFibroblastsHumansHypoxia-Inducible Factor 1, alpha SubunitIdiopathic Pulmonary FibrosisImmunohistochemistryIndolesPhenotypeRatsRNA-SeqSignal TransductionBleomycinHIF1A protein, humanHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitIndolesnintedanibbleomycinextracellular matrixfibrosisHIF1Ain-vivoIPFnintedanibPAI-1signaling

Identifiers

PMID33805152
PMCPMC8078165
OpenAlexW3136626802

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.