Victor Ruiz

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: The findings suggest that in IPF there is higher expression of TIMPs compared with collagenases, supporting the hypothesis that a nondegrading fibrillar collagen microenvironment is prevailing.

TL;DR: It is suggested that fibroblasts from IPF exhibit a profibrotic secretory phenotype, with lower growth rate and increased spontaneous apoptosis, which is similar to that seen in control lungs.

TL;DR: It is suggested that an imbalance between collagenases and TIMPs, excessive gelatinolytic activity, and epithelial apoptosis participate in the fibrotic response in this experimental model of pulmonary fibrosis induced in rats with paraquat and hyperoxia.

TL;DR: Fibrocytes express a variety of MMPs and that MMP-8 actively participates in the process of fibrocyte migration, as revealed by real-time polymerase chain reaction.