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

Kovacic, J. C., Dimmeler, S., Harvey, R. P., Finkel, T., Aikawa, E., Krenning, G. & Baker, A. H., 22-Jan-2019, In : Journal of the American College of Cardiology. 73, 2, p. 190-209 20 p.

Research output: Contribution to journalReview articleAcademicpeer-review

  • Jason C. Kovacic
  • Stefanie Dimmeler
  • Richard P. Harvey
  • Toren Finkel
  • Elena Aikawa
  • Guido Krenning
  • Andrew H. Baker

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.

Original languageEnglish
Pages (from-to)190-209
Number of pages20
JournalJournal of the American College of Cardiology
Volume73
Issue number2
Publication statusPublished - 22-Jan-2019

    Keywords

  • cardiovascular, EndMT, endothelial to mesenchymal transition, PROGENITOR CELLS, SMOOTH-MUSCLE, GENE-EXPRESSION, CORONARY VASCULATURE, DNA METHYLATION, ENDOCARDIAL FIBROELASTOSIS, PULMONARY-HYPERTENSION, REGULATORY MECHANISMS, EPIGENETIC REGULATION, SIGNALING PATHWAY

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