Carina Becerril

TL;DR: Findings suggest that there is an upregulation of collagenase 1 and 2 and gelatinases A and B, and an increase in endothelial and epithelial cell death, which may contribute to the pathogenesis of COPD through the remodeling of airways and alveolar structures.

TL;DR: A potential mechanism by which osteopontin secreted from the alveolar epithelium may exert a profibrotic effect in IPF lungs is provided and osteoponin is highlighted as a potential target for therapeutic intervention in this incurable disease.

TL;DR: In this paper, the authors evaluated evidence for the presence of fibrocytes in the lung of patients with idiopathic pulmonary fibrosis by immunofluorescence and confocal microscopy.

TL;DR: A subgroup of IPF patients, predominantly smoking males, display an accelerated clinical course and have a gene expression pattern that is different from those with slower progression and longer survival, which may explain the difficulty in obtaining significant and reproducible results in studies of therapeutic interventions in patients with IPF.

TL;DR: The findings indicate that the SHH pathway is activated in IPF lungs and that SHH may contribute to IPF pathogenesis by increasing the proliferation, migration, extracellular matrix production, and survival of fibroblasts.