Pulmonary artery hypertension (PAH) is a chronic and progressive disease that affects 15
persons per million. Although current therapy has improve disease prognosis, PAH still has a
poor survival, with a median survival of 2.8 years after diagnosis. In the last few years new
key elements in PAH pathogenesis have been discovered, such as the role of metabolism in
disease onset and progression. In fact, PAH pulmonary smooth muscle cells switch into a
glycolytic phenotype which resembles the metabolism of cancer cells. The investigators
hypothesis is that "fatty acid oxidation inhibition reverts the PAH adverse phenotype by
restoring mitochondrial function and morphology, decreasing proliferation and restoring
apoptosis susceptibility in pulmonary smooth muscle cells "
Phase:
Phase 2
Details
Lead Sponsor:
Pontificia Universidad Catolica de Chile
Collaborator:
Fondo Nacional de Desarrollo Científico y Tecnológico, Chile