Version 1
: Received: 11 May 2024 / Approved: 13 May 2024 / Online: 13 May 2024 (14:40:04 CEST)
How to cite:
Singh, A.; Bhatt, K. S.; Nguyen, H. C.; Frisbee, J. C.; Singh, K. K. Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology. Preprints2024, 2024050888. https://doi.org/10.20944/preprints202405.0888.v1
Singh, A.; Bhatt, K. S.; Nguyen, H. C.; Frisbee, J. C.; Singh, K. K. Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology. Preprints 2024, 2024050888. https://doi.org/10.20944/preprints202405.0888.v1
Singh, A.; Bhatt, K. S.; Nguyen, H. C.; Frisbee, J. C.; Singh, K. K. Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology. Preprints2024, 2024050888. https://doi.org/10.20944/preprints202405.0888.v1
APA Style
Singh, A., Bhatt, K. S., Nguyen, H. C., Frisbee, J. C., & Singh, K. K. (2024). Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology. Preprints. https://doi.org/10.20944/preprints202405.0888.v1
Chicago/Turabian Style
Singh, A., Jefferson C. Frisbee and Krishna K. Singh. 2024 "Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology" Preprints. https://doi.org/10.20944/preprints202405.0888.v1
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 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 cause and/or effect of EndMT to eventually target EndMT appears to be a promising strategy to treat aberrant EndMT-associated diseases. However, this approach is limited by a lack of precise functional and molecular pathways, causes and/or effects, and lack of robust animal model and human data about EndMT in different diseases. Here, we review different mechanisms in EndMT and the role of EndMT in various cardiovascular diseases.
Keywords
Endothelial to Mesenchymal Transition, EndMT, Mechanisms, Cardiovascular Diseases
Subject
Biology and Life Sciences, Biology and Biotechnology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
