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The role of endothelial-mesenchymal transition in development and pathological process
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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“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).”
From SOX9 reprograms endothelial cells by altering the chromatin landscape (2022) · cites this paper as [75]
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Metadata
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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