Vascular Remodeling: Just Say NO!

“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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