The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Role of the TGF-beta/Alk5 signaling pathway in monocrotaline-induced pulmonary hypertension.
Ari L Zaiman; Megan Podowski; Satya Medicherla; Kimberley Gordy; Fang Xu; Lijie Zhen; Larissa A Shimoda; Enid Neptune; Linda Higgins; Alison Murphy; et al. (Profiled Authors: Rubin Tuder; Enid Neptune; Larissa Shimoda; Hunter Champion; Ari Zaiman)
Johns Hopkins School of Medicine, Division of Pulmonary and Critical Care Medicine, 1830 East Monument Street, 5th Floor, Baltimore, MD 21205, USA. firstname.lastname@example.org
American journal of respiratory and critical care medicine 2008;177(8):896-905.
RATIONALE: Pulmonary arterial hypertension is a progressive disease characterized by an elevation in the mean pulmonary artery pressure leading to right heart failure and a significant risk of death. Alterations in two transforming growth factor (TGF) signaling pathways, bone morphogenetic protein receptor II and the TGF-beta receptor I, Alk1, have been implicated in the pathogenesis of pulmonary hypertension (PH). However, the role of TGF-beta family signaling in PH and pulmonary vascular remodeling remains unclear. OBJECTIVES: To determine whether inhibition of TGF-beta signaling will attenuate and reverse monocrotaline-induced PH (MCT-PH). METHODS: We have used an orally active small-molecule TGF-beta receptor I inhibitor, SD-208, to determine the functional role of this pathway in MCT-PH. MEASUREMENTS AND MAIN RESULTS: The development of MCT-PH was associated with increased vascular cell apoptosis, which paralleled TGF-beta signaling as documented by psmad2 expression. Inhibition of TGF-beta signaling with SD-208 significantly attenuated the development of the PH and reduced pulmonary vascular remodeling. These effects were associated with decreased early vascular cell apoptosis, adventitial cell proliferation, and matrix metalloproteinase expression. Inhibition of TGF-beta signaling with SD-208 in established MCT-PH resulted in a small but significant improvement in hemodynamic parameters and medial remodeling. CONCLUSIONS: These findings provide evidence that increased TGF-beta signaling participates in the pathogenesis of experimental severe PH.
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