Murine models of pulmonary fibrosis.

By B. Moore, C. Hogaboam. American Journal of Physiology - Lung cellular and Molecular Physiology, 2008

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Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression (2010, background): “1 A) and the myofibroblast marker –smooth muscle actin (-SMA; not depicted; Zhang et al., 1994; Pena et al., 2007; Moore and Hogaboam, 2008).”
Integrating mechanisms of pulmonary fibrosis (2011, background): “, asbestos and silica), radiation, bronchiolitis obliterans, and chronic graft-versus-host– induced pulmonary fibrosis, it remains unclear whether any of the experimental models truly duplicate the idiopathic form of the disease that is commonly seen in humans (Moore and Hogaboam, 2008).”
miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis (2010, methodology): “A miRNA array assay was performed on RNA isolated from the lungs of mice that had been given intratracheal PBS or bleomycin for 1 or 2 wk, a well-characterized model of lung fibrosis (Moore and Hogaboam, 2008).”
Reversal of Persistent Fibrosis in Aging by Targeting Nox4-Nrf2 Redox Imbalance (2014, background): “Preclinical animal models of lung fibrosis are largely used in young mice, which predominantly results in a self-limited fibrotic response (33, 34).”
Acellular normal and fibrotic human lung matrices as a culture system for in vitro investigation. (2012, background): “In part, this is due to the lack of an animal model that faithfully recapitulates the human disease (12).”