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Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology.
Singh, Aman; Bhatt, Kriti S; Nguyen, Hien C; Frisbee, Jefferson C; Singh, Krishna K.
Afiliação
  • Singh A; Department of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
  • Bhatt KS; Department of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
  • Nguyen HC; Department of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
  • Frisbee JC; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
  • Singh KK; Department of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
Int J Mol Sci ; 25(11)2024 Jun 04.
Article em En | MEDLINE | ID: mdl-38892367
ABSTRACT
Under different pathophysiological conditions, endothelial cells lose endothelial phenotype and gain mesenchymal cell-like phenotype via a process known as endothelial-to-mesenchymal transition (EndMT). At the molecular level, endothelial cells lose the expression of endothelial cell-specific markers such as CD31/platelet-endothelial cell adhesion molecule, von Willebrand factor, and vascular-endothelial cadherin and gain the expression of mesenchymal cell markers such as α-smooth muscle actin, N-cadherin, vimentin, fibroblast specific protein-1, and collagens. EndMT is induced by numerous different pathways triggered and modulated by multiple different and often redundant mechanisms in a context-dependent manner depending on the pathophysiological status of the cell. EndMT plays an essential role in embryonic development, particularly in atrioventricular valve development; however, EndMT is also implicated in the pathogenesis of several genetically determined and acquired diseases, including malignant, cardiovascular, inflammatory, and fibrotic disorders. Among cardiovascular diseases, aberrant EndMT is reported in atherosclerosis, pulmonary hypertension, valvular disease, fibroelastosis, and cardiac fibrosis. Accordingly, understanding the mechanisms behind the cause and/or effect of EndMT to eventually target EndMT appears to be a promising strategy for treating aberrant EndMT-associated diseases. However, this approach is limited by a lack of precise functional and molecular pathways, causes and/or effects, and a lack of robust animal models and human data about EndMT in different diseases. Here, we review different mechanisms in EndMT and the role of EndMT in various cardiovascular diseases.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doenças Cardiovasculares / Transição Epitelial-Mesenquimal Limite: Animals / Humans Idioma: En Revista: Int J Mol Sci Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Canadá

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doenças Cardiovasculares / Transição Epitelial-Mesenquimal Limite: Animals / Humans Idioma: En Revista: Int J Mol Sci Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Canadá