Evidence map›Paper›PMID 33371458›Full record

ReviewBiomedicines2020

Endothelial to Mesenchymal Transition in Pulmonary Vascular Diseases.

Eunsik Yun, Yunjin Kook, Kyung Hyun Yoo, Keun Il Kim, Myeong-Sok Lee, Jongmin Kim, Aram Lee

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology.International journal of molecular sciences · 2024
    Review
  18. Review
  19. Review
  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

7 authors at 1 institution in 1 country.

Eunsik YunDivision of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
Yunjin KookDivision of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
Kyung Hyun YooDivision of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.ORCID 0000-0003-2172-5564
Keun Il KimDivision of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
Myeong-Sok LeeDivision of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
Jongmin KimDivision of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
Aram LeeDivision of Biological Sciences, Sookmyung Women's University, Seoul 04310, Korea.
Sookmyung Women's University · KR

Funding

National Research Foundation of Korea NRF-2016R1A5A1011974National Research Foundation of Korea NRF-2019R1A2C4069815
6 · The paper itself

Abstract

Lung diseases, such as pulmonary hypertension and pulmonary fibrosis, are life-threatening diseases and have common features of vascular remodeling. During progression, extracellular matrix protein deposition and dysregulation of proteolytic enzymes occurs, which results in vascular stiffness and dysfunction. Although vasodilators or anti-fibrotic therapy have been mainly used as therapy owing to these characteristics, their effectiveness does not meet expectations. Therefore, a better understanding of the etiology and new therapeutic approaches are needed. Endothelial cells (ECs) line the inner walls of blood vessels and maintain vascular homeostasis by protecting vascular cells from pathological stimuli. Chronic stimulation of ECs by various factors, including pro-inflammatory cytokines and hypoxia, leads to ECs undergoing an imbalance of endothelial homeostasis, which results in endothelial dysfunction and is closely associated with vascular diseases. Emerging studies suggest that endothelial to mesenchymal transition (EndMT) contributes to endothelial dysfunction and plays a key role in the pathogenesis of vascular diseases. EndMT is a process by which ECs lose their markers and show mesenchymal-like morphological changes, and gain mesenchymal cell markers. Despite the efforts to elucidate these molecular mechanisms, the role of EndMT in the pathogenesis of lung disease still requires further investigation. Here, we review the importance of EndMT in the pathogenesis of pulmonary vascular diseases and discuss various signaling pathways and mediators involved in the EndMT process. Furthermore, we will provide insight into the therapeutic potential of targeting EndMT.

Indexed as

endothelial to mesenchymal transitionlung diseasepulmonary fibrosispulmonary hypertension

Identifiers

PMID33371458
PMCPMC7767472
OpenAlexW3116223290

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.