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Valvular endothelial cells and the mechanoregulation of valvular pathology.

Authors
  • Butcher, Jonathan T
  • Nerem, Robert M
Type
Published Article
Journal
Philosophical transactions of the Royal Society of London. Series B, Biological sciences
Publication Date
Aug 29, 2007
Volume
362
Issue
1484
Pages
1445–1457
Identifiers
PMID: 17569641
Source
Medline
License
Unknown

Abstract

Endothelial cells are critical mediators of haemodynamic forces and as such are important foci for initiation of vascular pathology. Valvular leaflets are also lined with endothelial cells, though a similar role in mechanosensing has not been demonstrated. Recent evidence has shown that valvular endothelial cells respond morphologically to shear stress, and several studies have implicated valvular endothelial dysfunction in the pathogenesis of disease. This review seeks to combine what is known about vascular and valvular haemodynamics, endothelial response to mechanical stimuli and the pathogenesis of valvular diseases to form a hypothesis as to how mechanical stimuli can initiate valvular endothelial dysfunction and disease progression. From this analysis, it appears that inflow surface-related bacterial/thrombotic vegetative endocarditis is a high shear-driven endothelial denudation phenomenon, while the outflow surface with its related calcific/atherosclerotic degeneration is a low/oscillatory shear-driven endothelial activation phenomenon. Further understanding of these mechanisms may help lead to earlier diagnostic tools and therapeutic strategies.

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