Thromboxane
Thromboxane is a member of the family of
Thromboxane is named for its role in blood clot formation (thrombosis).
Production
People with asthma tend to have increased thromboxane production, and analogs of thromboxane act as bronchoconstrictors in patients with asthma.[1]
Mechanism
Thromboxane acts by binding to any of the
Functions
Thromboxane is a
It is in
If the cap of a vulnerable plaque erodes or ruptures, as in myocardial infarction, platelets stick to the damaged lining of the vessel and to each other within seconds and form a plug. These "Sticky platelets" secrete several chemicals, including thromboxane A2 that stimulate vasoconstriction, reducing blood flow at the site.
Role of A2 in platelet aggregation
Thromboxane A2 (TXA2), produced by activated platelets, has prothrombotic properties, stimulating activation of new platelets as well as increasing platelet aggregation.
Platelet aggregation is achieved by mediating expression of the glycoprotein complex
Pathology
It is believed that the vasoconstriction caused by thromboxanes plays a role in
Thromboxane inhibitors
Thromboxane inhibitors are broadly classified as either those that inhibit the synthesis of thromboxane, or those that inhibit the target effect of it.
Thromboxane synthesis inhibitors, in turn, can be classified regarding which step in the synthesis they inhibit:
- The widely used drug aspirin acts by inhibiting the ability of the COX enzyme to synthesize the precursors of thromboxane within platelets. Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation. This anticoagulant property makes aspirin useful for reducing the incidence of heart attacks.[8] 40 mg of aspirin a day is able to inhibit a large proportion of maximum thromboxane A2 release provoked acutely, with the prostaglandin I2 synthesis being little affected; however, higher doses of aspirin are required to attain further inhibition.[9]
- thromboxane synthase) in the synthesis of thromboxane. Ifetroban is a potent and selective thromboxane receptor antagonist.[10] Dipyridamoleantagonizes this receptor too, but has various other mechanisms of antiplatelet activity as well.
- High-dose COX-1 and have been found to be associated "with a small but definite vascular hazard".[11]
The inhibitors of the target effects of thromboxane are the
Picotamide has activity both as a thromboxane synthase inhibitor and as a thromboxane receptor antagonist.[12]
Ridogrel is another example.[13]
References
- ISBN 9780123740014. Retrieved 20 January 2023.
- ^ Rat kidney thromboxane receptor: molecular cloning, signal ...
- S2CID 40932766.
- S2CID 27252438.
- PMID 16103291.
- .
- PMID 20503171.
- ^ [1] American Heart Association: Aspirin in Heart Attack and Stroke Prevention "The American Heart Association recommends aspirin use for patients who've had a myocardial infarction (heart attack), unstable angina, ischemic stroke (caused by blood clot) or transient ischemic attacks (TIAs or "little strokes"), if not contraindicated. This recommendation is based on sound evidence from clinical trials showing that aspirin helps prevent the recurrence of such events as heart attack, hospitalization for recurrent angina, second strokes, etc. (secondary prevention). Studies show aspirin also helps prevent these events from occurring in people at high risk (primary prevention)." [2]
- S2CID 14177039.
- PMID 10901709.
- PMID 23726390.
- PMID 9754941.
- PMID 1759039.
External links
- Thromboxanes at the U.S. National Library of Medicine Medical Subject Headings (MeSH)