Role of endothelial-mesenchymal transition (EndoMT) in the pathogenesis of fibrotic disorders
Open accessAbstract
The accumulation of a large number of myofibroblasts is responsible for exaggerated and uncontrolled production of extracellular matrix during the development and progression of pathological fibrosis. Myofibroblasts in fibrotic tissues are derived from at least three sources: expansion and activation of resident tissue fibroblasts, transition of epithelial cells into mesenchymal cells (epithelial-mesenchymal transition, EMT), and tissue migration of bone marrow-derived circulating fibrocytes. Recently, endothelial to mesenchymal transition (EndoMT), a newly recognized type of cellular transdifferentiation, has emerged as another possible source of tissue myofibroblasts. EndoMT is a complex biological process in which endothelial cells lose their specific markers and acquire a mesenchymal or myofibroblastic phenotype and express mesenchymal cell products such as α smooth muscle actin (α-SMA) and type I collagen. Similar to EMT, EndoMT can be induced by transforming growth factor (TGF-β). Recent studies using cell-lineage analysis have demonstrated that EndoMT may be an important mechanism in the pathogenesis of pulmonary, cardiac, and kidney fibrosis, and may represent a novel therapeutic target for fibrotic disorders.
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Fibrogenic myofibroblasts may also derive from portal fibroblasts, bone marrow-derived cells, circulating fibrocytes, and by epithelial-to-mesenchymal or endothelial-to-mesenchymal transition.
“they may also derive from portal fibroblasts, bone marrow-derived cells, circulating fibrocytes, [7] and by the controversially discussed epithelial-tomesenchymal (EMT) [8,9] or endothelial-to-mesenchymal (EndoTM) transition.[10,11]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [10]
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- Authors
- Piera-Velazquez, S., Li, Z., & Jimenez, S. A.
- Affiliations
- Thomas Jefferson University (US)
- ORCID
- Li, Zhaodong
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2011-09
- Volume
- 179
- Issue
- 3
- Pages
- 1074-1080
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC3157273
- OpenAlex
- W2125227867
- Cited by
- 580
- References
- 46
- Citations by year
- 2026: 16 · 2025: 29 · 2024: 40 · 2023: 29 · 2022: 37 · 2021: 45 · 2020: 42 · 2019: 50 · 2018: 52 · 2017: 48 · 2016: 47 · 2015: 46 · 2014: 37 · 2013: 31 · 2012: 28
- FWCI
- 2.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5 R01 AR19616)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- endothelial-to-mesenchymal transition, fibrosis, myofibroblasts, extracellular matrix synthesis, epithelial-mesenchymal transition, fibrocytes, TGF-beta, alpha-smooth muscle actin, type I collagen, pulmonary fibrosis, myocardial fibrosis, renal fibrosis, therapeutic target
- MeSH terms
- Animals, Cell Communication, Fibroblasts, Fibrosis, Humans, Kidney, Mesoderm, Myocardium, Pulmonary Fibrosis, Mice, Epithelial-Mesenchymal Transition
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