Reactive oxygen species are highly toxic molecules formed during a variety of physiological and pathological biochemical processes. Since they are highly reactive and extremely unstable, their reactions may lead to DNA damage, mitochondrial dysfunction, cell membrane damage, and eventually cell death. Oxidative stress results from an imbalance between anti- and pro-oxidants, and markers of oxidative stress can be found in many diseases, including brain injury in the course of stroke, congestive heart failure and coronary artery disease, lung damage in acute lung injury or ARDS (acute lung distress syndrome), acute kidney injury, and autoimmune inflammatory diseases.

Advances in molecular medicine have enabled us to identify the critical pathways involved in platelet activation. Furthermore, crucial regulators of these pathways (i.e., receptors and cytokines) have been identified, resulting in the development of novel strategies for the treatment of coronary artery disease. Nevertheless, further studies are required in order to establish an optimal strategy for prevention of platelet aggregation in subjects at increased risk thrombotic events. Considering that platelets play an important role in regulating vascular homeostasis, the analysis of changes in in their function will allow for the explanation of the key factors determining individual response to pharmacological interventions. It is well known that activation of the endothelium results in activation of platelets and that antiplatelet drugs improve endothelial function. Inhibition of platelet-dependent proinflammatory action in the vascular wall holds promise as a novel therapeutic strategy, however its precise molecular base remains unexplained. On the other hand, treatment aiming at improving endothelial function also exerts antiplatelet activity. Hence, studying the pharmacology of platelets cannot be separated from the pharmacology of the endothelium.

This Special Issue aims to collate both original research and review articles with a focus on the knowledge gained from studies performed on endothelium, combined with analysis of the function of platelets, allowing for the extensive investigation of the interaction between endothelium and platelets under various pathological conditions, both in in vitro and in vivo studies.

Potential topics include but are not limited to the following:

• Novel mechanisms regulating platelet-endothelium interactions, including nitric oxide biotransformation
• Oxidative stress as a major pathophysiological link between autoimmune diseases and cardiovascular disorders
• Hypoxia-reoxygenation in obstructive sleep apnoea as a modulator of endothelial and platelet function
• Changes in the endothelial and platelet phenotype in acute oxidative-stress-induced organ damage – new data
• Metabolic syndrome and diabetes – the molecular background for changes in platelet function
• potential biomarkers for the diagnosis and monitoring of chronic inflammatory disorders
• Influence of different diets, physical factors on endothelium and oxidative stress