Multiple stromal populations contribute to pulmonary fibrosis without evidence for epithelial to mesenchymal transition

By J. Rock, C. E. Barkauskas, Michael J. Cronce, Yan Xue, Jeffrey R. Harris, Jiurong Liang, P. Noble, B. Hogan. Proceedings of the National Academy of Sciences of the United States of America, 2011

959 citations recorded by the source corpus.

Subfields: Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/0a26608a25741c232d6536753dbab679fef30e16

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In Pulmonary and Respiratory Medicine

Citations in the corpus

Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis (2020, background): “Sometimes referred to as hyperplastic alveolar epithelial cells (25), these cells have been a source for controversy because they seemed to have acquired mesenchymal features and lost some epithelial features, suggesting active EMT (29), a finding not supported by lineage tracing experiments in anim”
Monocyte-derived alveolar macrophages drive lung fibrosis and persist in the lung over the life span (2017, background): “…of this trial and studies reporting that lung inflammation is sometimes worse in mice with genetic mutations that prevent the development of fibrosis, many concluded that inflammation is dispensable for the development of fibrosis (Munger et al., 1999; Budinger et al., 2006; Rock et al., 2011).”
Fibroblasts in fibrosis: novel roles and mediators (2014, methodology): “Using lineage tracing with recombinant td-Tomato and f-GFP tags and confocal microscopy resolution, Rock et al. demonstrated focal accumulation of fibroblasts derived from the proliferation of stromal cells (Rock et al., 2011).”
Cellular and molecular mechanisms in kidney fibrosis. (2014, positive): “Comparative studies from other organs suggest cells identified as resident fibroblasts in vivo have a close relationship with epithelium and may regulate epithelial functions and differentiation (40, 46).”
Type 2 alveolar cells are stem cells in adult lung. (2013, positive): “Mice were Sftpc-CreER T2 ; Scgb1a1-CreER TM ; and Rosa26R-CAG-tdTm (Rosa-Tm) (13); Rosa26R-CAG-Confetti (Rosa-Confetti ) (19) (supplied by and repair it after injury and to identify the signaling pathways that regulate these behaviors.”
Therapy for Fibrotic Diseases: Nearing the Starting Line (2013, background): “Injured epithelial cells have been considered a progenitor cell for myofibroblasts through EMT (20, 54, 147), but several fate mapping studies have failed to identify epithelial cells as a source of myofibroblasts in murine models of fibrosis in kidney, liver, and lung (125, 130, 133, 134, 137, 148)”
Fibroblasts: origins, definitions, and functions in health and disease (2021, background): “3864 Cell 184, July 22, 2021 Mouse studies have identified PDGFRa+/Axin2+ fibroblasts that respond to injury by proliferating within the alveolar niche and PDGFRa /Axin2+ fibroblasts that largely contribute to forming an anatomically distinct set of parabronchial myofibroblasts.”
TGF-β1 Signaling and Tissue Fibrosis. (2018, methodology): “(Rock et al. 2011).”
Single-cell RNA sequencing reveals profibrotic roles of distinct epithelial and mesenchymal lineages in pulmonary fibrosis (2019, background): “This stands in contrast to genetic lineage-tracing studies performed in mouse models of PF (34, 35).”