The Role of Platelet Dysfunctions in the Pathogenesis of the Hemostatic-Coagulant System Imbalances

Abstract

Platelet dysfunction plays a critical role in the pathogenesis of various disorders affecting the hemostatic-coagulant system. This review aims to explore the mechanisms by which platelet dysfunctions contribute to the disruption of hemostasis, leading to an increased risk of both thrombosis and bleeding. Platelets, traditionally known for their role in clot formation, can exhibit altered functionality under pathological conditions such as cardiovascular diseases, metabolic disorders, and autoimmune diseases, impacting their interaction with coagulation factors and vascular endothelium. The review discusses the molecular and cellular mechanisms underlying platelet dysfunction, including aberrations in platelet activation, aggregation, and secretion. It also highlights the interplay between platelets and other components of the coagulation cascade, such as fibrinogen and clotting factors, in maintaining vascular integrity. Moreover, the review examines clinical implications, including how platelet dysfunction can be a contributing factor in conditions like deep vein thrombosis, stroke, and disseminated intravascular coagulation (DIC). Finally, current therapeutic approaches targeting platelet dysfunctions, including antiplatelet agents and emerging therapies, are reviewed to provide insights into potential strategies for managing fluid-coagulation system imbalances. This review underscores the importance of a comprehensive understanding of platelet dysfunction to improve diagnosis and treatment of hemostatic disorders.

Keywords: hemostasis; platelet dysfunction; the hemostatic-coagulant system; thrombosis.

Figure 1

Schematic representation of primary hemostasis: platelet adhesion at the site of vascular injury, mediated by von Willebrand factor, which binds to GP Ib-IX receptors, followed by platelet aggregation through fibrinogen bridges bound to GP IIb-IIIa receptors, ultimately leading to the formation of the platelet thrombus.