How does platelet aggregation work?
Platelet aggregation, the process by which platelets adhere to each other at sites of vascular injury, has long been recognized as critical for hemostatic plug formation and thrombosis.
What is the ligand for the P2Y12 receptor?
ATP, 2-meSATP and ATP-γ-S have been reported to both stimulate and antagonise the P2Y12 receptor….Contents:
Description: | Structure of the human P2Y12 receptor in complex with an antithrombotic drug |
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Ligand: | AZD1283 |
Resolution: | 2.62Å |
Species: | Human |
References: | 63 |
What is the mechanism of platelets?
Platelets, which circulate within the blood, are the essential mediators that trigger the mechanical pathway of the coagulation cascade upon encountering any damage to the blood vessels. Platelets encourage primary hemostasis via three major processes: activation, adhesion and aggregation.
What causes platelet degranulation?
Platelet degranulation within a PTCA-damaged vessel would be increased by a nonionic contrast medium, releasing procoagulant molecules and platelet-derived growth factors into the damaged vessel lumen, which might contribute to acute thrombosis and the initiation of the restenosis process.
What is a P2Y12 platelet function test?
Test results are in P2Y12 reaction units (PRU). This test measures the extent of platelet aggregation in the presence of P2Y12 inhibitor drugs such as clopidogrel (Plavix), prasugrel (Effient), ticagrelor (Brilinta) and ticlopidine (Ticlid).
How does Plavix work in the body?
Clopidogrel works by blocking platelets from sticking together and prevents them from forming harmful clots. It is an antiplatelet drug. It helps keep blood flowing smoothly in your body.
How does ADP cause platelet aggregation?
Acting through cell surface receptors, ADP activates platelets resulting in shape change, aggregation, thromboxane A2 production, and release of granule contents.
How does clopidogrel work on platelets?
Clopidogrel slows the blood’s clotting action by making platelets less sticky. Platelets are blood cells that stick together to block cuts and breaks in blood vessels. But if you’re at risk of heart attack or stroke, platelets can stick together inside already narrowed blood vessels to form a clot.
What induces platelet aggregation?
Substances such as collagen, ristocetin, arachidonic acid, adenosine 5′-diphosphate, epinephrine, and thrombin can stimulate platelets and hence induce aggregation. Response to these aggregating agents (known as agonists) provides a diagnostic pattern for different disorders of platelet function.
What triggers platelet adhesion and aggregation?
Depending on the matrix proteins exposed to blood and the hemodynamic conditions, platelet adhesion requires the synergistic function of different platelet receptors, ultimately leading to platelet activation and aggregation.
When do platelets Degranulate?
Basically after about 60 s of stimulation dependent on the agonist, platelets are either fully degranulated, or their remaining granules are centralized.
How does aspirin inhibit platelet aggregation?
Abstract. The antithrombotic action of aspirin (acetylsalicylic acid) is due to inhibition of platelet function by acetylation of the platelet cyclooxygenase (COX) at the functionally important amino acid serine529.
Where is P2Y12 found in platelets?
In the field of purinergic signaling, the P2Y12 protein on the periphery is found mainly but not exclusively on the surface of blood platelets, and is an important regulator in blood clotting.
How do P2Y12 inhibitors work?
P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor) act as antagonists of the platelet adenosine diphosphate receptor P2Y12, thereby inhibiting platelet aggregation.
What is the function of P2Y12 receptor?
The P2Y12 receptor is the predominant receptor involved in the ADP-stimulated activation of the glycoprotein IIb/IIIa receptor [10]. Activation of the glycoprotein IIb/IIIa receptor results in enhanced platelet degranulation and thromboxane production, and prolonged platelet aggregation [11].
What is the importance of inhibition of platelet aggregation?
Inhibition of platelet aggregation by medical treatment impairs formation and progression of thrombotic processes and is therefore of great importance in the prevention of complications after an ACS or around PCI [2, 3].