Vol 18, No 4 (2011)
Review Article
Published online: 2011-07-15
Novel therapeutic targets for preserving a healthy endothelium: Strategies for reducing the risk of vascular and cardiovascular disease
Cardiol J 2011;18(4):352-363.
Abstract
The endothelium lies in a strategic anatomical position between the circulating blood and the
vascular smooth-muscle cells. It is a source of vasodilators such as nitric oxide, prostacyclin,
and hyperpolarizing factor as well as heparin-like substances and other molecules with antiproliferative
properties. These effects of endothelial cells may explain why platelets and
monocytes usually do not adhere at the blood vessel wall. However, under pathological conditions,
endothelial dysfunction occurs and significantly contributes to the increase of platelet-
-vessel wall interaction, vasoconstriction, pro-inflammation, and proliferation. Under these
conditions, endothelium-dependent vasodilation is reduced, and endothelium-dependent constrictor
responses are augmented. Upon vessel wall injury, the platelets rapidly adhere to the
exposed sub-endothelial matrix, which is mediated by several cellular receptors present on
platelets or endothelial cells and various adhesive proteins. Subsequent platelet activation
results in the recruitment of additional platelets and the generation of platelet aggregates, so
forming a stable platelet plug. Therapeutic strategies aimed at improving or preserving endothelial
function therefore may be promising in terms of preventing and treating coronary
artery disease. Diagnostic modalities for assessing endothelial function should allow for the
early detection of vascular endothelial dysfunction before the manifestation of serious adverse
vascular disorders. (Cardiol J 2011; 18, 4: 352–363)
Keywords: vascularendothelial cellcardiovascular disorderscoronary syndromevasoconstrictionvasodilationinflammationanti-inflammationanti-plateletpro-plateletanti-coagulantpro-coagulantdiagnosis of endothelial function