Evidence map›Paper›PMID 25971970›Full record

ArticleThe Journal of biological chemistry2015

Snail Is a Direct Target of Hypoxia-inducible Factor 1α (HIF1α) in Hypoxia-induced Endothelial to Mesenchymal Transition of Human Coronary Endothelial Cells.

Xingbo Xu, Xiaoying Tan, Björn Tampe, Elisa Sanchez, Michael Zeisberg, Elisabeth M Zeisberg

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

114 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Roles of the Altitude-Adapted Immune Microenvironment in Pulmonary Vascular Remodeling in High-Altitude Pulmonary Hypertension: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
  11. Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  12. Article
  13. Review
  14. COL8A1 regulates endothelial phenotype in inflammatory endothelial-to-mesenchymal transition.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  15. Review
  16. Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology.International journal of molecular sciences · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Review

54 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Xingbo XuFrom the Departments of Cardiology and Pneumology and.
Xiaoying TanFrom the Departments of Cardiology and Pneumology and.
Björn TampeNephrology and Rheumatology, University Medical Center of Göttingen, Georg August University, 37075 Göttingen, Germany and.
Elisa SanchezFrom the Departments of Cardiology and Pneumology and.
Michael ZeisbergNephrology and Rheumatology, University Medical Center of Göttingen, Georg August University, 37075 Göttingen, Germany and.
Elisabeth M ZeisbergFrom the Departments of Cardiology and Pneumology and DZHK (German Centre for Cardiovascular Research) partner site, 37075 Göttingen, Germany elisabeth.zeisberg@med.uni-goettingen.de.
University of Göttingen · DEGerman Centre for Cardiovascular Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial to mesenchymal transition (EndMT) was originally described in heart development where the endocardial endothelial cells that line the atrioventricular canal undergo an EndMT to form the endocardial mesenchymal cushion that later gives rise to the septum and mitral and tricuspid valves. In the postnatal heart specifically, endothelial cells that originate from the endocardium maintain increased susceptibility to undergo EndMT as remnants from their embryonic origin. Such EndMT involving adult coronary endothelial cells contributes to microvascular rarefaction and subsequent chronification of hypoxia in the injured heart, ultimately leading to cardiac fibrosis. Although in most endothelial beds hypoxia induces tip cell formation and sprouting angiogenesis, here we demonstrate that hypoxia is a stimulus for human coronary endothelial cells to undergo phenotypic changes reminiscent of EndMT via a mechanism involving hypoxia-inducible factor 1α-induced activation of the EndMT master regulatory transcription factor SNAIL. Our study adds further evidence for the unique susceptibility of endocardium-derived endothelial cells to undergo EndMT and provides novel insights into how hypoxia contributes to progression of cardiac fibrosis. Additional studies may be required to discriminate between distinct sprouting angiogenesis and EndMT responses of different endothelial cells populations.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCells, CulturedEndocardiumEndothelial CellsHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMiceMice, Inbred C57BLSnail Family Transcription FactorsTranscription FactorsHypoxia-Inducible Factor 1, alpha SubunitSnail Family Transcription FactorsTranscription Factorsendothelial cellfibroblastfibrosishypoxiahypoxia-inducible factor (HIF)

Identifiers

PMID25971970
PMCPMC4505417
OpenAlexW782467378

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.