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A thrombus in the cerebral arteries refers to a pathological blood clot that forms within or embolizes to the arterial supply of the brain, leading to acute ischemic stroke [1]. It is not a single molecular target but a complex biological structure composed of a fibrin meshwork, activated platelets, and trapped red and white blood cells [4]. The formation of such a thrombus obstructs cerebral blood flow, resulting in oxygen deprivation and rapid neuronal death in the affected territory [2]. In clinical practice, the thrombus is the primary focus of acute intervention, where thrombolytic drugs like Alteplase are used to chemically dissolve the fibrin structure [3]. Additionally, mechanical thrombectomy may be employed to physically retrieve the thrombus from the vessel. Prevention of thrombus recurrence involves pharmacological targeting of the coagulation cascade and platelet function using anticoagulants and antiplatelets [1].
Thrombolytic agents (plasminogen activators) bind to fibrin within the thrombus and convert entrapped plasminogen to plasmin, which enzymatically degrades the fibrin matrix to dissolve the clot [1]. Antiplatelet agents inhibit specific enzymes (e.g., COX-1) or receptors (e.g., P2Y12) to prevent platelet activation and aggregation [3]. Anticoagulants interfere with the coagulation cascade (e.g., inhibiting Factor Xa or Thrombin) to prevent the formation and propagation of fibrin strands [4].
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