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J Am Coll Cardiol. 2019 Jan 22;73(2):190-209. doi: 10.1016/j.jacc.2018.09.089.

Endothelial to Mesenchymal Transition in Cardiovascular Disease: JACC State-of-the-Art Review.

Author information

1
The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: jason.kovacic@mountsinai.org.
2
Institute for Cardiovascular Regeneration, Goethe University, and German Center of Cardiovascular Research, Frankfurt, Germany.
3
Developmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia; St. Vincent's Clinical School and School of Biotechnology and Biomolecular Science, University of New South Wales, Kensington, New South Wales, Australia.
4
Aging Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
5
Center for Interdisciplinary Cardiovascular Sciences, and Center for Excellence in Vascular Biology, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
6
Laboratory for Cardiovascular Regenerative Medicine, Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
7
UoE/BHF Center for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh, United Kingdom. Electronic address: Andy.Baker@ed.ac.uk.

Abstract

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.

KEYWORDS:

EndMT; cardiovascular; endothelial to mesenchymal transition

PMID:
30654892
DOI:
10.1016/j.jacc.2018.09.089
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