TY - JOUR
T1 - Endothelial to Mesenchymal Transition in Cardiovascular Disease JACC State-of-the-Art Review
T2 - JACC State-of-the-Art Review
AU - Kovacic, Jason C.
AU - Dimmeler, Stefanie
AU - Harvey, Richard P.
AU - Finkel, Toren
AU - Aikawa, Elena
AU - Krenning, Guido
AU - Baker, Andrew H.
N1 - Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.
PY - 2019/1/22
Y1 - 2019/1/22
N2 - Endothelial to mesenchymal transition (EndMT) is a process whereby an endothelial cell undergoes a series of molecular events that lead to a change in phenotype toward a mesenchymal cell (e.g., myofibroblast, smooth muscle cell). EndMT plays a fundamental role during development, and mounting evidence indicates that EndMT is involved in adult cardiovascular diseases (CVDs), including atherosclerosis, pulmonary hypertension, valvular disease, and fibroelastosis. Therefore, the targeting of EndMT may hold therapeutic promise for treating CVD. However, the field faces a number of challenges, including the lack of a precise functional and molecular definition, a lack of understanding of the causative pathological role of EndMT in CVDs (versus being a "bystander-phenomenon"), and a lack of robust human data corroborating the extent and causality of EndMT in adult CVDs. Here, we review this emerging but exciting field, and propose a framework for its systematic advancement at the molecular and translational levels. (J Am Coll Cardiol 2019; 73: 190-209) (c) 2019 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.
AB - Endothelial to mesenchymal transition (EndMT) is a process whereby an endothelial cell undergoes a series of molecular events that lead to a change in phenotype toward a mesenchymal cell (e.g., myofibroblast, smooth muscle cell). EndMT plays a fundamental role during development, and mounting evidence indicates that EndMT is involved in adult cardiovascular diseases (CVDs), including atherosclerosis, pulmonary hypertension, valvular disease, and fibroelastosis. Therefore, the targeting of EndMT may hold therapeutic promise for treating CVD. However, the field faces a number of challenges, including the lack of a precise functional and molecular definition, a lack of understanding of the causative pathological role of EndMT in CVDs (versus being a "bystander-phenomenon"), and a lack of robust human data corroborating the extent and causality of EndMT in adult CVDs. Here, we review this emerging but exciting field, and propose a framework for its systematic advancement at the molecular and translational levels. (J Am Coll Cardiol 2019; 73: 190-209) (c) 2019 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.
KW - cardiovascular
KW - EndMT
KW - endothelial to mesenchymal transition
KW - PROGENITOR CELLS
KW - SMOOTH-MUSCLE
KW - GENE-EXPRESSION
KW - CORONARY VASCULATURE
KW - DNA METHYLATION
KW - ENDOCARDIAL FIBROELASTOSIS
KW - PULMONARY-HYPERTENSION
KW - REGULATORY MECHANISMS
KW - EPIGENETIC REGULATION
KW - SIGNALING PATHWAY
U2 - 10.1016/j.jacc.2018.09.089
DO - 10.1016/j.jacc.2018.09.089
M3 - Review article
C2 - 30654892
SN - 0735-1097
VL - 73
SP - 190
EP - 209
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 2
ER -