TY - JOUR
T1 - Non-coding RNA in endothelial-to-mesenchymal transition
AU - Hulshoff, Melanie S.
AU - Del Monte-Nieto, Gonzalo
AU - Kovacic, Jason
AU - Krenning, Guido
N1 - Funding Information:
G.K. received support from the Netherlands Organization for Scientific Research/Netherlands Organization for Health Research and Development Innovational Research Incentive #917.16.446. G.d.M.-N.’s research is supported by a Future Leader Fellowship (102036) from the National Heart Foundation of Australia, a Discovery Project (DP190101475) from the Australian Research Council, and start-up funds from Monash University. M.H. received support from a Graduate School of Medical Sciences (GSMS) PhD scholarship, University of Groningen. J.K. acknowledges research support from the National Institutes of Health (R01HL130423 and R01HL135093).
Publisher Copyright:
© The Author(s) 2019.
PY - 2019/10/1
Y1 - 2019/10/1
N2 - Endothelial-to-mesenchymal transition (EndMT) is the process wherein endothelial cells lose their typical endothelial cell markers and functions and adopt a mesenchymal-like phenotype. EndMT is required for development of the cardiac valves, the pulmonary and dorsal aorta, and arterial maturation, but activation of the EndMT programme during adulthood is believed to contribute to several pathologies including organ fibrosis, cardiovascular disease, and cancer. Non-coding RNAs, including microRNAs, long non-coding RNAs, and circular RNAs, modulate EndMT during development and disease. Here, we review the mechanisms by which non-coding RNAs facilitate or inhibit EndMT during development and disease and provide a perspective on the therapeutic application of non-coding RNAs to treat fibroproliferative cardiovascular disease.
AB - Endothelial-to-mesenchymal transition (EndMT) is the process wherein endothelial cells lose their typical endothelial cell markers and functions and adopt a mesenchymal-like phenotype. EndMT is required for development of the cardiac valves, the pulmonary and dorsal aorta, and arterial maturation, but activation of the EndMT programme during adulthood is believed to contribute to several pathologies including organ fibrosis, cardiovascular disease, and cancer. Non-coding RNAs, including microRNAs, long non-coding RNAs, and circular RNAs, modulate EndMT during development and disease. Here, we review the mechanisms by which non-coding RNAs facilitate or inhibit EndMT during development and disease and provide a perspective on the therapeutic application of non-coding RNAs to treat fibroproliferative cardiovascular disease.
KW - Cardiac development
KW - Cardiovascular disease
KW - Endothelial-mesenchymal transition (EndMT)
KW - Non-coding RNA
KW - Plasticity
UR - http://www.scopus.com/inward/record.url?scp=85072588360&partnerID=8YFLogxK
U2 - 10.1093/cvr/cvz211
DO - 10.1093/cvr/cvz211
M3 - Review article
C2 - 31504268
AN - SCOPUS:85072588360
SN - 0008-6363
VL - 115
SP - 1716
EP - 1731
JO - Cardiovascular Research
JF - Cardiovascular Research
IS - 12
ER -
