Atherosclerosis: Endothelial Dysfunction and Beyond

Dear Colleagues,

Endothelial dysfunction, a recognized antecedent of atherosclerotic plaques, is associated with reduced bioavailability of nitric oxide (NO), a key endogenous anti-atherogenic molecule. The magnitude of endothelial dysfunction predicts future adverse cardiovascular events both in the general population and patients with risk factors or atherosclerotic cardiovascular (CV) disease. Beyond direct effects within the vessel wall, the L-arginine-NO pathway modulates the activity of pathophysiologic contributors to acute coronary syndromes and stroke, i.e., platelets, the coagulation and fibrinolytic pathways, and the immune system. Additionally, impaired NO bioavailability accelerates adverse CV remodelling in aging, hypertension, diabetes, and heart failure. Recent years have witnessed expanding research on the role of NO and other endothelial mediators in a variety of common disorders, including metabolic syndrome, chronic kidney disease, and heart failure with preserved ejection fraction. Moreover, improved endothelial function may be implicated in beneficial pleiotropic effects of new antidiabetic, antiplatelet, and anticoagulant drugs. On the other hand, there is no consensus with regard to the utility of particular endothelial biomarkers in specific clinical settings. With this Special Issue, we hope to encourage submissions of original articles and reviews covering novel aspects of atherogenesis and endothelial dysfunction, with a focus on emerging CV risk factors, the L-arginine-NO system, and related metabolic pathways.

We look forward to receiving your submission.

Prof. Dr. Andrzej Surdacki
Prof. Dr. Dimitrios Tsikas
Guest Editors

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