Cited by 177Cancer Cells and MetastasisTGF-β signaling in diseasesMesenchymal stem cell research

The role of endothelial-mesenchymal transition in development and pathological process

Lin, Feng, Wang, Nan, Zhang, Tong‐Cun·2012·IUBMB Life

Abstract

Epithelial-mesenchymal transition is an important developmental process, participates in tumor's formation, invasion, and metastasis and has been extensively studied. Recently, endothelial-mesenchymal transition (EndMT), a newly recognized type of cellular transdifferentiation, has been demonstrated to participate in a number of diseases by causing morphology changes and pathological processes. Previous studies showed that EndMT was a critical process of embryonic cardiac development. Not only that recent advances also suggested that EndMT occurred postnatally in cancer and cardiac fibrosis and emerged as a possible source of cancer-associated fibroblasts (CAFs). CAFs were found to acquire properties that promoted tumor development and metastasis formation. Resident endothelial cells undergoing EndMT lose their endothelial markers, acquire a mesenchymal or myofibroblastic phenotype, express mesenchymal cell products such as α-smooth muscle actin and type I collagen and develop invasive and migratory abilities. EndMT-derived cells are believed to function as fibroblasts in damaged tissue and may therefore have an important role in pathological process. However, little is known about the signaling mechanisms that cause endothelial cells to transform into mesenchymal cells. Transforming growth factor-β, Notch, or other signaling pathways could direct or interact to mediate EndMT. Therefore, to explore the signaling mechanisms of EndMT may provide novel therapeutic strategies for…

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Crossref · 10.1002/iub.1059

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  • Tissue damage may stimulate EndMT to give rise to fibroblasts during wound healing or fibrotic diseases and EndMT forms cancer-associated fibroblasts in the tumor microenvironment, which regulates disease progression.

    “Tissue damage may stimulate EndMT to give rise to fibroblasts during wound healing or fibrotic diseases and EndMT forms cancer-associated fibroblasts in the tumor microenvironment, which regulates disease progression (75).”

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Authors
Lin, F., Wang, N., & Zhang, T.
Affiliations
Tianjin University of Science and Technology (CN)
Corresponding author
Wang, Nan
Venue
IUBMB Life
Publisher
Wiley
Published
2012-06-25
Volume
64
Issue
9
Pages
717-723
ISSN
  • 1521-6543 (ISSN-L)
  • 1521-6551
OpenAlex
W1996010478
Cited by
177
References
49
Citations by year
2026: 1 · 2025: 5 · 2024: 7 · 2023: 12 · 2022: 14 · 2021: 16 · 2020: 13 · 2019: 17 · 2018: 20 · 2017: 32 · 2016: 19 · 2015: 13 · 2014: 3 · 2013: 5
FWCI
0.69
Type
journal article
Language
en
Open access
closed
Locations
  • IUBMB Life (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Science Foundation
  • National Natural Science Foundation of China
  • Natural Science Foundation of Tianjin City
Topics
  • Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
  • Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
Keywords
endothelial-to-mesenchymal transition, epithelial-mesenchymal transition, cancer-associated fibroblasts, myocardial fibrosis, embryonic heart development, tumor invasion and metastasis, TGF-beta signaling, Notch signaling, endothelial cells, myofibroblastic phenotype, signaling mechanisms
MeSH terms
Animals, Fibrosis, Heart Diseases, Humans, Neoplasms, Regeneration, Signal Transduction, Disease Progression, Embryonic Development, Cell Transdifferentiation

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