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Habashi, Jennifer P; Judge, Daniel P; Holm, Tammy M; Cohn, Ronald D; Loeys, Bart L; Cooper, Timothy K; Myers, Loretha; Klein, Erin C; Liu, Guosheng; Calvi, Carla; Podowski, Megan; Neptune, Enid R; Halushka, Marc K; Bedja, Djahida; Gabrielson, Kathleen; Rifkin, Daniel B; Carta, Luca; Ramirez, Francesco; Huso, David L; Dietz, Harry C
Science (American Association for the Advancement of Science), 04/2006, Letnik: 312, Številka: 5770Journal Article
Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-{szligbeta} (TGF-{szligbeta}) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-{szligbeta} signaling and can be prevented by TGF-{szligbeta} antagonists such as TGF-{szligbeta}-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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