Endothelial-to-mesenchymal transition (EndMT) is characterized by multiple morphological and physiological changes, including loss of endothelial cell polarity, disruption of intercellular junctions, migration, altered extracellular matrix secretion, and increased proliferation. EndMT is a fundamental process during early development, however, it has been identified in a multitude of cardiovascular disease processes such as progressive atherosclerotic plaques, valvular heart disease, myocardial infarction, pulmonary hypertension, and cardiac fibrosis and remodeling in heart failure. Evidence for EndMT in these disease processes is observed strongly in human pathologies, implying the clinical relevance of EndMT in cardiovascular diseases.
EndMT entails a spectrum of cell phenotypic changes in which endothelial cells (ECs) downregulate their adhesion junction molecules (e.g. CD31, VECAD) and upregulate contractile and invasive markers (e.g. SMA, nCAD, CNN1). During development and in the process of transition, ECs delaminate from an organized cell layer and invade the underlying tissue. However, there is less understanding of these processes in the post-development stages, especially during the pathogenesis of cardiovascular diseases.
Furthermore, in vitro observations suggest that EndMT can exhibit myofibroblast-like properties by producing markers such as as collagen I, vimentin, and fibroblast-specific protein-1. In addition to that, EndMT has been shown to play a role in the pathogenesis of diseases by locally releasing a spectrum of cytokines and proteases. EndMT is thus a complex physiologic state and there are dramatic cellular and molecular changes required for the EndMT to occur. However, there is little evidence on the regulation of EndMT formation, its mechanism of action, and the extent of EndMT contribution in the pathogenesis of cardiovascular diseases.
In this Research Topic, we seek to provide scope on the most recent and cutting-edge discoveries on the molecular mechanism of EndMT and its contribution to the development of cardiovascular diseases.
Potential topics may include but are not limited to the following questions:
1) How EndMT develops and contributes to the pathogenesis of cardiovascular diseases.
2) Novel strategies to detect the EndMT in vivo.
3) Experimental and clinical evidence on the role(s) of EndMT in the development and complications of cardiovascular diseases.
4) Molecular pathway(s) of EndMT in different cardiovascular diseases.
Endothelial-to-mesenchymal transition (EndMT) is characterized by multiple morphological and physiological changes, including loss of endothelial cell polarity, disruption of intercellular junctions, migration, altered extracellular matrix secretion, and increased proliferation. EndMT is a fundamental process during early development, however, it has been identified in a multitude of cardiovascular disease processes such as progressive atherosclerotic plaques, valvular heart disease, myocardial infarction, pulmonary hypertension, and cardiac fibrosis and remodeling in heart failure. Evidence for EndMT in these disease processes is observed strongly in human pathologies, implying the clinical relevance of EndMT in cardiovascular diseases.
EndMT entails a spectrum of cell phenotypic changes in which endothelial cells (ECs) downregulate their adhesion junction molecules (e.g. CD31, VECAD) and upregulate contractile and invasive markers (e.g. SMA, nCAD, CNN1). During development and in the process of transition, ECs delaminate from an organized cell layer and invade the underlying tissue. However, there is less understanding of these processes in the post-development stages, especially during the pathogenesis of cardiovascular diseases.
Furthermore, in vitro observations suggest that EndMT can exhibit myofibroblast-like properties by producing markers such as as collagen I, vimentin, and fibroblast-specific protein-1. In addition to that, EndMT has been shown to play a role in the pathogenesis of diseases by locally releasing a spectrum of cytokines and proteases. EndMT is thus a complex physiologic state and there are dramatic cellular and molecular changes required for the EndMT to occur. However, there is little evidence on the regulation of EndMT formation, its mechanism of action, and the extent of EndMT contribution in the pathogenesis of cardiovascular diseases.
In this Research Topic, we seek to provide scope on the most recent and cutting-edge discoveries on the molecular mechanism of EndMT and its contribution to the development of cardiovascular diseases.
Potential topics may include but are not limited to the following questions:
1) How EndMT develops and contributes to the pathogenesis of cardiovascular diseases.
2) Novel strategies to detect the EndMT in vivo.
3) Experimental and clinical evidence on the role(s) of EndMT in the development and complications of cardiovascular diseases.
4) Molecular pathway(s) of EndMT in different cardiovascular diseases.