Alveolar epithelial cell mesenchymal transition develops in vivo during pulmonary fibrosis and is regulated by the extracellular matrix

By Kevin K. Kim, M. Kugler, P. Wolters, L. Robillard, M. Galvez, A. Brumwell, D. Sheppard, H. Chapman. Proceedings of the National Academy of Sciences of the United States of America, 2006

1,313 citations recorded by the source corpus.

Subfields: Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/edc36e8339d96606ac96c437dc701927c3f4b868

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In Pulmonary and Respiratory Medicine

1. Jeremy S. Duffield
2. M. Nieto
3. J. P. Thiery
4. B. Hogan
5. J. Rock
6. S. Friedman
7. P. Noble
8. R. Huang

Citations in the corpus

• TGF-β-induced EMT: mechanisms and implications for fibrotic lung disease (2007, methodology): “Furthermore, mouse AT2 cell cultures on fibronectin or fibrin were shown to undergo EMT via integrin-dependent activation of endogenous latent TGF- 1 (45).”
• Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix (2007, neutral): “, 2007) involving αvβ6 integrin– mediated latent TGF-β1 activation (Kim et al., 2006).”
• Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “While themajority of studies on fibrosis have been carried out in the kidney, the same pathways are likely to operate during other fibrotic processes, including those in the liver and the lung, especially since there is evidence of EMT in hepatic fibrosis (Kim et al, 2006; Zeisberg et al, 2007a).”
• Epithelial-mesenchymal transitions in development and disease. (2009, background): “, 2007b), as do the alveolar epithelial cells during the pulmonary fibrosis induced by TGFβ (Kim et al., 2006).”
• Multiple stromal populations contribute to pulmonary fibrosis without evidence for epithelial to mesenchymal transition (2011, methodology): “They argue against a major direct contribution of epithelial cells to fibroblast foci through the process of EMT.”
• Therapy for Fibrotic Diseases: Nearing the Starting Line (2013, background): “The use of anti-inflammatory drugs in suppressing or reversing fibrosis Cell death Pathologic EMT TGFβ activation Immune responses Inflammation Toxins Cell stress ER stress ROS Innate lymphoid cells Extracellular matrix Myofibroblasts T cells Macrophages Infection (viruses and bacteria)Trauma Pro-fi”
• Fibrosis and adipogenesis originate from a common mesenchymal progenitor in skeletal muscle (2011, background): “However, many recent studies have indicated that the origins of J o u rn a l o f C e ll S c ie n c e ECM-producing cells in multiple organs and tissues are diverse and complex (Friedman, 2000; Iwano et al., 2002; Kim et al., 2006; Lin et al., 2008; Zeisberg et al., 2007b).”
• Reciprocal regulation of TGF-β and reactive oxygen species: A perverse cycle for fibrosis (2015, neutral): “TGF-β is the most potent inducer of EMT and can induce EMT in epithelial cells from different organs in vitro and in vivo [84,90,101,218,219,227 – 230].”
• TGF-β1 Signaling and Tissue Fibrosis. (2018, methodology): “Identification of costaining cells is suggestive of EMT, but has inherent limitations (Kakugawa et al. 2005; Willis et al. 2005; Kim et al. 2006).”
• Epithelial repair mechanisms in the lung. (2010, background): “- and MMP-2 Stimulation of wound repair (90) Lung BE biopsies - and EMT Induction of EMT in lungs following overexpression of TGF (78) Triple transgenic mouse and adenoviral expression of TGF- and EMT, with -catenin Induction of EMT (83) 1° rat ATII Smad3 & transgelin Stimulation of migration (197) ”