Endothelial to mesenchymal transition: A novel therapeutic target for cardiovascular diseases

Abstract Endothelial to mesenchymal transition (EndMT) is a complex biological process in which endothelial cells lose their specific markers and acquire a mesenchymal or myofibroblastic phenotype. Similar to epithelial-mesenchymal transition (EMT), EndMT can be induced by multiple stimulants such a...

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Bibliographic Details
Published in:Trends in cardiovascular medicine 2017-08, Vol.27 (6), p.383-393
Main Authors: Jackson, Ampadu O, Zhang, Jingjing, Jiang, Zhisheng, Yin, Kai
Format: Article
Language:English
Subjects:
Animals
Atherosclerosis
Biomarkers - metabolism
Cardiovascular
Cardiovascular diseases
Cardiovascular Diseases - metabolism
Cardiovascular Diseases - pathology
Cardiovascular Diseases - physiopathology
Cardiovascular Diseases - therapy
Cardiovascular system
Cell adhesion & migration
Cytokines
EndMT
Endothelial cells
Endothelial Cells - metabolism
Endothelial Cells - pathology
Endothelium
Endothelium, Vascular - metabolism
Endothelium, Vascular - pathology
Endothelium, Vascular - physiopathology
Epithelial-Mesenchymal Transition
Fibroblasts
Fibrosis
Fibrotic disorders
Genotype & phenotype
Growth factors
Heart
Humans
Mesenchyme
Metabolism
Molecular modelling
Pathogenesis
Phenotype
Physiology
Pulmonary hypertension
Roles
Signal Transduction
Smooth muscle
Stem cells
Stimulants
Systems development
Transcription factors
Vascular Remodeling
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Summary:Abstract Endothelial to mesenchymal transition (EndMT) is a complex biological process in which endothelial cells lose their specific markers and acquire a mesenchymal or myofibroblastic phenotype. Similar to epithelial-mesenchymal transition (EMT), EndMT can be induced by multiple stimulants such as cytokines and metabolic factors that play crucial roles in the development of the cardiovascular system. Recent studies have demonstrated that EndMT may play a significant role in the pathogenesis of cardiovascular diseases (CVDs), and may represent a novel therapeutic target for cardiovascular remodeling and fibrotic disorders. The exact molecular mechanisms involved in cardiovascular pathogenesis that occur as a result of EndMT, however, are not fully explained. In this review, we reveal the multiple intercellular mechanisms of EndMT including stimulants, signaling pathways, and seek to explore the relationship between this biological process, cardiovascular system development, and CVDs that may lead to new therapeutic strategies for the treatment of CVDs.
ISSN:1050-1738
1873-2615
DOI:10.1016/j.tcm.2017.03.003