fibrinogeenbridging

Fibrinogen bridging is a process in hemostasis and thrombosis in which circulating fibrinogen molecules help connect platelets to one another, promoting platelet aggregation. In this view, a single fibrinogen molecule can bind simultaneously to receptors on two adjacent platelets, acting as a molecular bridge that stabilizes an forming thrombus.

Mechanism: When platelets are activated by vascular injury, glycoprotein IIb/IIIa receptors on their surfaces adopt high‑affinity conformations and bind to the gamma and other binding sites of fibrinogen. As a result, one fibrinogen molecule can link two platelets, drawing them into close contact and reinforcing aggregation. Fibrinogen bridging often occurs in concert with other adhesive interactions, such as platelet adhesion to exposed subendothelial structures, but its cross‑linking role is a key driver of early platelet cohesion.

Clinical relevance: Fibrinogen bridging is fundamental to normal clot formation, but excessive bridging can contribute to pathological thrombosis. Pharmacologic blockade of GP IIb/IIIa receptors disrupts fibrinogen bridging and reduces platelet aggregation, an approach used in certain acute coronary settings and during some interventional procedures to limit thrombotic risk.

Variations and implications: Abnormal fibrinogen levels or structural variants can alter bridging efficiency and thrombus stability. Hyperfibrinogenemia may enhance bridging and thrombus growth, while hypofibrinogenemia or dysfibrinogenemia can impair bridging and hemostasis.

Overall, fibrinogen bridging describes a central mechanism by which fibrinogen links platelets to promote stable platelet aggregates, balancing the processes of normal hemostasis and thrombosis and serving as a target for antiplatelet therapies.