Formation of blood clots is an essential defence mechanism against mechanical injury, but inappropriate clotting is a major cause of heart attacks and strokes. In September 6 Nature, Gilberto Sambrano and colleagues from University of California at San Francisco, show that the protein thrombin is necessary for normal blood clotting, and receptors activated by it may be an important target in the treatment of thrombosis.

Sambrano et al. examined platelets from mice deficient in protease–activated receptor-4 (PAR-4 — a thrombin receptor) and found that these platelets fail to change shape, mobilize calcium, secrete ATP or aggregate in response to thrombin. In addition, PAR-4 deficient mice had increased bleeding times but did not develop thrombosis (Nature 2001, 413: 74-78).

"These results have implications for developing drugs to prevent cardiovascular problems and strokes," commented Skip Brass from the University of Pennsylvania in an accompanying News & Views article.

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