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Endothelium to Mesenchymal Transition—Contributions to Vascular Diseases

  • Marian Wesseling*
  • *Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceeding › Chapter › Academic › peer-review

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 languageEnglish
Title of host publicationEndothelium and Cardiovascular Diseases
Subtitle of host publicationVascular Biology and Clinical Syndromes
PublisherElsevier
Pages205-219
Number of pages15
ISBN (Electronic)9780443240362
ISBN (Print)9780443240379
DOIs
Publication statusPublished - 1 Jan 2025

Keywords

  • Angiogenesis
  • Atherosclerosis
  • Cardiovascular
  • Endothelial-to-mesenchymal transition
  • Fibrosis
  • TGF-β

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