What is the thidoxane A2?
Thromboxane A2 is a member of a group of lipids known as eikosanoids that act as signaling molecules in the human body. The thromboxan family also includes thromboxane B2. Activated plates use enzyme thromboxane-and synthase to convert prostaglandin H2 into thromboxane A2. Lipid then helps the formation of a clot by stimulating the activation of multiple platelets, increasing their aggregation and action as vasoconstrictive for narrow blood vessels. Many anticoagulation drugs act either against the formation or function of this molecule. Eikosanoids serve as signaling molecules for body processes such as smooth muscle contraction, clot formation, inflammation and contraction of uterus. The Thovoxane A2 is a key part of the formation of the clot and the Tromboxane B2 is its inactive metabolite. Because the active form is very unstable, scientists of the tromboxan test levels B2 as an indication of thromboxan production A2 during research studies. Cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2)reactions in which arachidone is converted into prostaglandins. Prostaglandin H2 is the predecessor of Tromboxan A2.
During the process of clot creation, the thrombin plates activate at the point of injury. The thromboxane-A synthase enzyme, which is present in activated platelet, converts prostaglandin H2 into thromboxane A2. This molecule then activates more platelets and creates a loop of positive feedback that forms a clot of blood. Lipid also causes the injured blood vessel to reduce, which further inhibits bleeding.
Because this molecule is so important for the creation of a clot, it is the goal of many Anticoagulant's drug. For example, aspirin irreversibly inactivates cox enzymes and prevents thromboxan from producing the production of prostaglandin H2. Other non -steroidal anti -inflammatory drugs (NSAIDs) such as ibuprofen also reversely inactivate cox enzymes. Some anticoagulants inhibit thromBoxane-A synthase and others are thromboxan receptor antagonists A2.
The creation of clots has been most understood from the A2 thromboxan functions since the beginning of 2011, but the activities of eicosanoids and their interaction with other molecules in the body are very complex. Some studies suggest that it could interact with thrombin to stimulate the proliferation of new smooth muscle cells in the damaged artery walls, dealing with an active role in repairing blood vessels. Other studies have found that receptors for this molecule in the thyroid gland can play a role in apoptosis (programmed cellular death) of certain cells in the thymus. Tymocyte apoptosis is associated with immune problems and low survival in patients who have sepsis, so further study in this area could prove to be valuable to care for these patients.
TROMBOXANE A2 receptors are abundant in the lungs and spleen, as well as the thymus and function of the molecules in these organs are still misunderstood. Another intense study function of the receptor in differentCH organs and eikosanoid interactions with other molecules are likely to illuminate the complex roles that this important molecule plays in the human body. This knowledge could be invaluable in the development of new drugs.