Tissue plasminogen activator

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Tissue plasminogen activator (tPA) is a serine protease found on endothelial cells associated with the blood vessels. As an enzyme, it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown. tPA is used in some cases of diseases that feature blood clots, such as pulmonary embolism and stroke, in a medical treatment called thrombolysis.

Tissue Plasminogen Activator Spinning Animation

Function[edit | edit source]

tPA is produced by the endothelium of blood vessels and has a role in the breakdown of blood clots (fibrinolysis). Its primary function is to convert plasminogen to plasmin. Plasmin is then able to degrade fibrin, the main component of blood clots. In this way, tPA is vital in the regulation of blood clotting, and, through this mechanism, it can also play a role in the cascade of events involved in cell migration and tissue remodeling.

Medical use[edit | edit source]

tPA is used in medicine to break down blood clots in a treatment known as thrombolysis. It is given through the veins (intravenous) or directly into the artery (intra-arterial). It is used in some cases of diseases that feature blood clots, such as an acute ischemic stroke, pulmonary embolism, and deep vein thrombosis.

Side effects[edit | edit source]

The most common side effect of tPA is bleeding. This can range from minor bleeding, such as nosebleeds, to life-threatening bleeding in the brain (intracranial hemorrhage). Other side effects can include allergic reactions, such as swelling of the lips and tongue (angioedema), and low blood pressure (hypotension).

History[edit | edit source]

tPA was first discovered in the 1970s and was initially produced using recombinant DNA technology. The first tPA drug, alteplase, was approved by the Food and Drug Administration (FDA) in 1987.

See also[edit | edit source]

Tissue plasminogen activator Resources
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