Abstract
Platelets and platelet microparticles (PMPs) play a key role in the pathophysiology of vascular disorders such as coronary artery disease and stroke. In atherosclerosis, for example, the disruption of the plaque exposes endogenous agonists such as collagen, which activates platelets. Platelet hyper-activation and the high levels of PMPs generated in such situations pose a thrombotic risk that can lead to strokes or myocardial infarctions. Interestingly, dietary polyphenols are gaining much attention due to their potential to mimic the antiplatelet activity of treatment drugs such as aspirin and clopidogrel that target the glycoprotein VI (GPVI)–collagen and cyclooxygenease-1 (COX-1)–thromboxane platelet activation pathways respectively. Platelet function tests such as aggregometry and flow cytometry used to monitor the efficacy of antiplatelet drugs can also be used to assess the antiplatelet potential of dietary polyphenols. Despite the low bioavailability of polyphenols, several in vitro and dietary intervention studies have reported antiplatelet effects of polyphenols. This review presents a summary of platelet function in terms of aggregation, secretion, activation marker expression, and PMP release. Furthermore, the review will critically evaluate studies demonstrating the impact of polyphenols on aggregation and PMP release.
Highlights
In Australia, despite decreasing deaths and hospitalization rates, cardiovascular diseases remain a major disease burden [1]
In situations where the blood vessel wall is damaged due to trauma or atherosclerotic plaque disruption, the platelets adhere to the vessel wall, leading to receptor activation, conformational change, degranulation, and aggregation [11]
This platelet adhesion is facilitated by von Willebrand factor (vWF) forming a bridge between the glycoprotein (GP) IIb/IIIa receptor and exposed collagen of the vessel wall [15]
Summary
In Australia, despite decreasing deaths and hospitalization rates, cardiovascular diseases remain a major disease burden [1]. Platelets are anucleate fragments of a larger cell—the megakaryocyte—that play a major role in the pathophysiology of such conditions [3] They are similar to most cells in that they have receptors that respond to extracellular signals, contain mitochondria and other organelles, and release bioactive compounds [3]. In situations where the blood vessel wall is damaged due to trauma or atherosclerotic plaque disruption, the platelets adhere to the vessel wall, leading to receptor activation, conformational change, degranulation, and aggregation [11] This platelet adhesion is facilitated by vWF forming a bridge between the glycoprotein (GP) IIb/IIIa ( referred to as integrin αIIbβ or CD41/CD61) receptor and exposed collagen of the vessel wall [15]. Platelet aggregation is achieved by crosslinking of adjacent platelets via fibrinogen or vWF bound to the GP IIb/IIIa receptor
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