Platelet-Collagen Interactions in Hemostatic Mechanisms.

Collagen exposure after endothelial disruption functions as a critical molecular signal for platelet adhesion and activation, which in turn supports thrombin generation and fibrin formation. As the extracellular matrix's predominant constituent, collagen provides the fundamental surface for clotting initiation. The interactions of specific platelet receptors with collagen are central to initiating and maintaining hemostasis. These receptors include glycoprotein VI (GPVI), the glycoprotein Ib-IX-V complex, and integrins such as α2β1 and αIIbβ3, with von Willebrand factor serving as a key ligand. However, systematic reviews of these specific receptor collagen interactions are relatively scarce. Although considerable progress has been made in elucidating these mechanisms, ongoing research continues to uncover additional regulatory complexity. This review systematically examines the binding mechanisms, signaling pathways, and functional roles of GPVI, vWF, and integrins in thrombus formation. This review also examines the role of other collagen types, such as types IV, VI, XV, and XVIII, in maintaining vascular integrity and supporting hemostasis. Finally, we highlight current research limitations and future directions, underscoring the need to validate collagen receptor interactions experimentally and develop novel antithrombotic therapies that target these pathways.