About this Research Topic
Platelets represent an important link between inflammation and thrombosis. Platelets are highly reactive components of the circulatory system, which exert not only haemostatic activity but also contribute to the modulation of various pathological conditions. Thus, defective activation of platelets causes uncontrolled bleeding and, conversely, platelet activation causes thrombotic disorders. Multiple pathways contribute to platelet activation, including those triggered by arachidonic acid, whose modulation or inhibition may result. It has been reported that arachidonic acid (AA) metabolism (PGHS or LOX pathways) participate in a sequence of events including platelet adhesion, activation, secretion and aggregation. Mitochondrial dysfunction contributes to the undesirable activation and aggregation of platelets being on the base of multiple pathologies. In addition, Protein Disulfide Isomerase (PDI) has also been reported to participate in some of these physiological and pathophysiological actions, e.g. activation of NADPH oxidase with an increase in platelet oxidative stress. The development of novel inhibitors of AA- pathways as well as PDI is an area of continuous study whose purpose is to avoid undesirable platelet activation and their analysis is the aim of this research topic.
Keywords: PDI, Platelets, NOX, Arachidonic acid
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