Evidence map›Paper›PMID 30864875›Full record

ReviewPhysiological reviews2019

Endothelial to Mesenchymal Transition: Role in Physiology and in the Pathogenesis of Human Diseases.

Sonsoles Piera-Velazquez, Sergio A Jimenez

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Physiological reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 394 papers.

0numbers the graph read from it
0cells of the map it votes in
394citing papers in PubMed
21.2field-weighted citation impact, top 1% 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

394 citing papers in PubMed, 632 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Glycoside fraction from pear seed functionally antagonizes sFLT-1 and restores angiogenic signaling in preeclampsia.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

334 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

2 authors at 2 institutions in 1 country.

Sonsoles Piera-VelazquezJefferson Institute of Molecular Medicine, Thomas Jefferson University , Philadelphia, Pennsylvania.
Sergio A JimenezJefferson Institute of Molecular Medicine, Thomas Jefferson University , Philadelphia, Pennsylvania.
Jefferson Institute · USThomas Jefferson University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies have demonstrated that endothelial cells are capable of undergoing endothelial to mesenchymal transition (EndMT), a newly recognized type of cellular transdifferentiation. EndMT is a complex biological process in which endothelial cells adopt a mesenchymal phenotype displaying typical mesenchymal cell morphology and functions, including the acquisition of cellular motility and contractile properties. Endothelial cells undergoing EndMT lose the expression of endothelial cell-specific proteins such as CD31/platelet-endothelial cell adhesion molecule, von Willebrand factor, and vascular-endothelial cadherin and initiate the expression of mesenchymal cell-specific genes and the production of their encoded proteins including α-smooth muscle actin, extra domain A fibronectin, N-cadherin, vimentin, fibroblast specific protein-1, also known as S100A4 protein, and fibrillar type I and type III collagens. Transforming growth factor-β1 is considered the main EndMT inducer. However, EndMT involves numerous molecular and signaling pathways that are triggered and modulated by multiple and often redundant mechanisms depending on the specific cellular context and on the physiological or pathological status of the cells. EndMT participates in highly important embryonic development processes, as well as in the pathogenesis of numerous genetically determined and acquired human diseases including malignant, vascular, inflammatory, and fibrotic disorders. Despite intensive investigation, many aspects of EndMT remain to be elucidated. The identification of molecules and regulatory pathways involved in EndMT and the discovery of specific EndMT inhibitors should provide novel therapeutic approaches for various human disorders mediated by EndMT.

Indexed as

DiseaseAnimalsEmbryonic DevelopmentEpithelial-Mesenchymal TransitionHumans

Identifiers

PMID30864875
PMCPMC6734087
OpenAlexW2920994691

What Socratic 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 Socratic graph.