Evidence map›Paper›PMID 29515588›Full record

ReviewFrontiers in immunology2018

Endothelial to Mesenchymal Transition Represents a Key Link in the Interaction between Inflammation and Endothelial Dysfunction.

Jin Gu Cho, Aram Lee, Woochul Chang, Myeong-Sok Lee, Jongmin Kim

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed
10.9field-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

177 citing papers in PubMed, 275 citations in OpenAlex.

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  12. Single-Cell Metabolic Imaging Reveals Glycogen-Driven Adaptations in Endothelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  13. Subclinical Changes in Cardiovascular Function During the Neonatal Period in Infants Born to Mothers With Diabetes.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2026
    Article
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  17. Observational
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  20. COL8A1 regulates endothelial phenotype in inflammatory endothelial-to-mesenchymal transition.American journal of physiology. Heart and circulatory physiology · 2025
    Article

117 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

5 authors at 2 institutions in 1 country.

Jin Gu ChoDivision of Biological Sciences, Sookmyung Women's University, Seoul, South Korea.
Aram LeeDivision of Biological Sciences, Sookmyung Women's University, Seoul, South Korea.
Woochul ChangDepartment of Biology Education, College of Education, Pusan National University, Busan, South Korea.
Myeong-Sok LeeDivision of Biological Sciences, Sookmyung Women's University, Seoul, South Korea.
Jongmin KimDivision of Biological Sciences, Sookmyung Women's University, Seoul, South Korea.
Sookmyung Women's University · KRPusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells that line the inner walls of blood vessels are in direct contact with blood and display remarkable heterogeneity in their response to exogenous stimuli. These ECs have unique location-dependent properties determined by the corresponding vascular beds and play an important role in regulating the homeostasis of the vascular system. Evidence suggests that vascular endothelial cells exposed to various environments undergo dynamic phenotypic switching, a key biological program in the context of endothelial heterogeneity, but that might result in EC dysfunction and, in turn, cause a variety of human diseases. Emerging studies show the importance of endothelial to mesenchymal transition (EndMT) in endothelial dysfunction during inflammation. EndMT is a complex biological process in which ECs lose their endothelial characteristics, acquire mesenchymal phenotypes, and express mesenchymal cell markers, such as alpha smooth muscle actin and fibroblast-specific protein 1. EndMT is induced by inflammatory responses, leading to pathological states, including tissue fibrosis, pulmonary arterial hypertension, and atherosclerosis,

Indexed as

Cell TransdifferentiationEndothelial CellsHumansInflammationVascular Diseasesendothelial dysfunctionendothelial heterogeneityendothelial to mesenchymal transitioninflammatory processvascular disease

Identifiers

PMID29515588
PMCPMC5826197
OpenAlexW2793749910

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.