Endothelial function: a critical determinant in atherosclerosis?

By Ulf Landmesser, Burkhard Hornig, Helmut Drexler. Circulation, 2004

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NADPH Oxidases in Cardiovascular Health and Disease (2006, background): “Increased NADPH oxidase-derived O2 • may also contribute to endothelial dysfunction in heart failure, where the ensuing vascular dysfunction may contribute to increased loading of the heart and reduced exercise tolerance (186).”
The Vascular Endothelium and Human Diseases (2013, background): “In these conditions, the endothelial phenotype changes to a proinflammatory and prothrombotic state (64) by increased expression of leukocyte adhesion molecules (such as VCAM-1) and cytokines such as monocyte chemoattractant protein-1.”
The role of shear stress in the pathogenesis of atherosclerosis (2005, background): “3 In addition, many risk factors linked to cardiovascular disease such as hypertension, smoking, hyperlipidemia, hyperhomocysteinemia and diabetes mellitus have a direct impact on endothelial cell functio”
Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice (2016, background): “S12), we conclude that changes in vasomotor function are likely the result of a complex interplay between nitric oxide bioavailability originating from the intima and oxidation state of sGC or downstream signal transduction molecules within the media (Landmesser et al., 2004; Feletou & Vanhoutte, 20”