Evidence map›Paper›PMID 35681530›Full record

ReviewCells2022

The Role of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease.

Qianman Peng, Dan Shan, Kui Cui, Kathryn Li, Bo Zhu, Hao Wu, Beibei Wang, Scott Wong, Vikram Norton, Yunzhou Dong and 3 more

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.4field-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

28 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  7. Review
  8. Store-operated CaAmerican journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  9. Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension.International journal of molecular sciences · 2025
    Review
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  15. Article
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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

13 authors at 2 institutions in 1 country.

Qianman PengVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0003-1854-0710
Dan ShanVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Kui CuiVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Kathryn LiVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Bo ZhuVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Hao WuVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Beibei WangVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Scott WongVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Vikram NortonVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Yunzhou DongVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Yao Wei LuVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0001-6200-2974
Changcheng ZhouDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, CA 92521, USA.
Hong ChenVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Boston Children's Hospital · USUniversity of California, Riverside · US

Funding

Epsin in Angiogenesis and Vascular RemodelingR01HL093242 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CHEN, HONG, WANG, DA-ZHI · 2009 to 2021
$7.3M
Molecular Mechanisms Controlling Lymphatic Vascular Function in Health and DiseaseR01HL133216 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, DIXON, JAMES BRANDON · 2016 to 2025
$6.7M
Mechanisms regulating VEGF receptors in diabetic angiogenesisR01HL130845 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, XU, JIAN · 2016 to 2023
$4.9M
Molecular Regulation of AtherosclerosisR01HL146134 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SRIVASTAVA, SANJAY · 2019 to 2022
$3.3M
CD45-mediated endothelial-to-mesenchymal transition in cardiovascular diseaseR01HL141853 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, WANG, DA-ZHI · 2020 to 2023
$3.3M
The role of signaling adaptor protein epsin in atherosclerosisR01HL156362 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SHI, JINJUN · 2021 to 2024
$3.1M
Molecular Mechanisms Regulating Neuropilin 2 in LymphangiogenesisR01HL141858 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI BIELENBERG, DIANE RENEE, CHEN, HONG · 2019 to 2022
$3.1M
The Role of Adaptor Protein Disabled-2 in Maintaining Endothelial Cell Function in AtherosclerosisR01HL162367 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SHI, JINJUN · 2022 to 2025
$3.0M
Molecular Mechanisms Governing Vascular Cell Function and Phenotype in Health and DiseaseR01HL158097 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, CHEN, YABING · 2021 to 2024
$3.0M
Endocrine disruptor mediated activation of PXR causes dyslipidemia and atherosclerosisR01ES023470 · NIEHS · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2013 to 2022
$2.7M
Molecular Mechanisms Regulating Endothelial DysfunctionR01HL137229 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SRIVASTAVA, SANJAY · 2017 to 2020
$2.7M
The Role of Signaling Adaptor Protein Epsin in AtherosclerosisR01HL118676 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CHEN, HONG · 2014 to 2017
$1.8M
BLRD VA I01 BX004426NHLBI NIH HHS R01 HL093242NHLBI NIH HHS R01 HL118676NHLBI NIH HHS R01 HL130845NHLBI NIH HHS R01 HL131925NHLBI NIH HHS R01 HL133216NHLBI NIH HHS R01 HL137229NHLBI NIH HHS R01 HL141853NHLBI NIH HHS R01 HL146134NHLBI NIH HHS R01 HL156362NHLBI NIH HHS R01 HL158097NHLBI NIH HHS R01 HL162367NIEHS NIH HHS R01 ES023470
6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition (EndoMT) is the process of endothelial cells progressively losing endothelial-specific markers and gaining mesenchymal phenotypes. In the normal physiological condition, EndoMT plays a fundamental role in forming the cardiac valves of the developing heart. However, EndoMT contributes to the development of various cardiovascular diseases (CVD), such as atherosclerosis, valve diseases, fibrosis, and pulmonary arterial hypertension (PAH). Therefore, a deeper understanding of the cellular and molecular mechanisms underlying EndoMT in CVD should provide urgently needed insights into reversing this condition. This review summarizes a 30-year span of relevant literature, delineating the EndoMT process in particular, key signaling pathways, and the underlying regulatory networks involved in CVD.

Indexed as

Cardiovascular DiseasesHypertension, PulmonaryEndothelial CellsEndotheliumEpithelial-Mesenchymal TransitionHumanscardiovascular diseasecell signalingendothelial-to-mesenchymal transitionmultidisciplinary and novel approaches

Identifiers

PMID35681530
PMCPMC9180466
OpenAlexW4281720842

What Socratic 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 Socratic graph.