Abstract
Severely dysfunctional endothelial cells (EC) can undergo endothelial-to-mesenchymal transition (EndoMT), losing EC characteristics and gaining mesenchymal cell phenotype and function. EndoMT can be induced by a large variety of inflammatory triggers, where transforming growth factor-β is the most potent and critical factor. EndoMT contributes to fibrosis, disrupting tissue homeostasis, reorganization, and adaptation of normal cardiovascular architecture. It is well-established that ECs play a major role in the onset and progression of cardiovascular disease. While EndoMT is known to be pivotal in prenatal cardiovascular development, recent emphasis has been placed on its role in postnatal vascular dysfunction. Major risk factors associated with cardiovascular disease can directly or indirectly trigger endothelial dysfunction, subsequently leading to EndoMT. This addresses the potential significant contribution of EndoMT to the onset and mechanism of vascular disease.
| Original language | English |
|---|---|
| Title of host publication | Endothelium and Cardiovascular Diseases |
| Subtitle of host publication | Vascular Biology and Clinical Syndromes |
| Publisher | Elsevier |
| Pages | 205-219 |
| Number of pages | 15 |
| ISBN (Electronic) | 9780443240362 |
| ISBN (Print) | 9780443240379 |
| DOIs | |
| Publication status | Published - 1 Jan 2025 |
Keywords
- Angiogenesis
- Atherosclerosis
- Cardiovascular
- Endothelial-to-mesenchymal transition
- Fibrosis
- TGF-β
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