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Freezing fibrosis at the source

Hyperactive skin cells cause fibrosis, but targets to prevent their pathogenic activation have been hard to pin down, thus making it difficult to intervene early in disease. Now, a European team has mapped out a pathway involving serotonin released by activated platelets that drives early steps in scleroderma, a form of dermal fibrosis.1

The findings could open up fibrotic disease as a therapeutic category for terguride, a serotonin receptor antagonist that Pfizer Inc. in-licensed from Ergonex Pharma GmbH last year. The platelet connection also could build the case for Amira Pharmaceuticals Inc.'s strategy of targeting receptors for platelet-derived inflammatory mediators to treat fibrotic diseases.

Fibrosis involves scarring and hardening of affected tissue due to deposition of extracellular matrix proteins by fibroblasts. Previous studies have found signs of inflammation and autoimmunity around fibrotic

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