“You are only as old as your endothelium”, as often stated by Paul M Vanhoutte, when
opening his famous “Mechanisms of Vasodilation” meetings from 1980 onwards, highlights
the importance of endothelium and the continuous process of vascular remodeling
in many physiological and pathophysiological situations as embryogenesis, wound healing,
tumor growth and ischemic disease. In chronic and acute cardiovascular occlusive
disease, different types of vascular remodeling contribute to tissue repair and vascular
growth. Firstly, collateral growth represents the expansive growth of preexisting vessels,
forming collateral bridges between arterial networks. Secondly, neovascularization refers
to vascular growth from a combination of three different mechanisms: vasculogenesis
is the formation of blood vessels by endothelial progenitors while angiogenesis refers
to capillary sprouting or intussusceptive growth and arteriogenesis to the subsequent
stabilization of these new vascular structures by mural cells1. Distinct, but partially overlapping,
cellular and molecular pathways drive collateral growth and neovascularization
(Figure 1)2. Hypoxia is known to stimulate neovascularization in the setting of ischemia,
whereas fluid shear stress (FSS) might be the most important trigger for initiation of
collateral growth. Besides these specific initial triggers, all types of vascular remodeling
share growth factors, chemokines, proteases, and inflammatory cells, which play different
roles in promoting and refining these processes.
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