Project details


Endothelial-Mesenchymal Transition in Cardiovascular Disease

microRNA epigenetics signal transduction

dr. G. Krenning
dr. J.A.J. Moonen

Nature of the research:
This is a fundamental research project where the mechanisms underlying Endothelial-Mesenchymal Transition and its contribution to cardiovascular diseases is investigated. Mechanisms under study are, signal transduction pathways, epigenetic influences, microRNAs, and biomechanical clues. Diseases under study are Cardiac Fibrosis/Heart Failure, (juvenile) Pulmonary Arterial Hypertension (PAH), Atherosclerosis and Aneurysms.

Fields of study:
medical biology molecular biology vascular medicine

Background / introduction
Endothelial-Mesenchymal Transition (EndMT) is a process wherein endothelial cells lose their endothelial phenotype and functions and acquire a mesenchymal (i.e. myofibroblast-like) phenotype. EndMT has been associated with a variety of cardiovascular diseases, however its relative contribution has not yet been established. During cardiac fibrosis, a large number of myofibroblasts are derived through EndMT by currently unknown mechanisms. Likewise, in atherosclerosis EndMT contributes to neointima formation, worsening atherosclerosis progression.
Research question / problem definition
In this project we aim to elucidate the underlying mechanisms of Endothelial-Mesenchymal Transition. Mechanisms under study are epigenetics, signal transduction cascades, microRNAs and biomechanical stimuli.
PMID: 20635395
PMID: 20083576
PMID: 22739237
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