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Remedying pulmonary vascular remodeling
Alterations in bone morphogenetic protein, growth and differentiation factor (GDF), and transforming growth factor–β signaling contribute to vascular remodeling and elevated pulmonary blood pressure in pulmonary arterial hypertension (PAH) and experimental pulmonary hypertension (PH). Yung et al. used a fusion protein to inhibit activin A/B and GDF8/11, ligands increased in PAH and PH tissues that signal through ACTRIIA to promote maladaptive vascular cell phenotypes. Treating rodent models of PH with the fusion protein reduced pulmonary artery pressure, pulmonary arteriolar muscularization and occlusion, right ventricular hypertrophy, and cell proliferation in the lungs. Results suggest that the fusion protein may help treat PH by reversing pathologic vascular remodeling.
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