Platelets are central to the process of wound healing. But overly responsive platelets could block normal blood flow, particularly where atherosclerosis exists, resulting in stroke, myocardial infarction and unstable angina. Hence the interest in studying the receptors for platelet-activating substances released from damaged vessels, like ADP.

In 11 January Nature, Pamela B. Conley of COR Therapeutics, California, and colleagues report that they have cloned the ADP receptor P2Y12 and showed that a patient with a bleeding disorder has a defect in this gene (Nature 2001, 409:202-207). This receptor is the target of efficacious antithrombotic agents such as ticlopidine and clopidrogel. The cloning of the P2Y12 receptor should thus facilitate the development of even better agents to treat cardiovascular disease.

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