Research Topic

From Arachidonic Acid to Protein Disulfide Isomerase: Key Targets for Anti-Platelet Therapy

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


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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28 May 2019 Manuscript

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Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

28 May 2019 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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