Animal models of fibrotic lung disease.
Bethany B. Moore,William Lawson,William Lawson,Tim D. Oury,Thomas H. Sisson,Krishnan Raghavendran,Cory M. Hogaboam +6 more
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TLDR
Each of the models reviewed in this report offers a powerful tool for studying some aspect of fibrotic lung disease and has a much better understanding of the fact that the aged lung has increased susceptibility to fibrosis.Abstract:
Interstitial lung fibrosis can develop as a consequence of occupational or medical exposure, as a result of genetic defects, and after trauma or acute lung injury leading to fibroproliferative acute respiratory distress syndrome, or it can develop in an idiopathic manner. The pathogenesis of each form of lung fibrosis remains poorly understood. They each result in a progressive loss of lung function with increasing dyspnea, and most forms ultimately result in mortality. To better understand the pathogenesis of lung fibrotic disorders, multiple animal models have been developed. This review summarizes the common and emerging models of lung fibrosis to highlight their usefulness in understanding the cell–cell and soluble mediator interactions that drive fibrotic responses. Recent advances have allowed for the development of models to study targeted injuries of Type II alveolar epithelial cells, fibroblastic autonomous effects, and targeted genetic defects. Repetitive dosing in some models has more closely mimicked the pathology of human fibrotic lung disease. We also have a much better understanding of the fact that the aged lung has increased susceptibility to fibrosis. Each of the models reviewed in this report offers a powerful tool for studying some aspect of fibrotic lung disease.read more
Citations
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Human placental mesenchymal stem cells of fetal origins-alleviated inflammation and fibrosis by attenuating MyD88 signaling in bleomycin-induced pulmonary fibrosis mice
Feng Li,Fei Han,Hui Li,Jia Zhang,Xia Qiao,Juan Shi,Li Yang,Jianda Dong,Meihui Luo,Jun Wei,Xiaoming Liu +10 more
TL;DR: The results showed an alleviated pulmonary inflammation and fibrosis in myeloid differentiation primary response gene 88-deficient mice treated with bleomycin (BLM), accompanied with a reduced TGF-β signaling and production of pro-fibrotic cytokines, including TNF-α, IL-1β.
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Systematic phenotyping and correlation of biomarkers with lung function and histology in lung fibrosis
Isis E. Fernandez,Oana V. Amarie,Kathrin Mutze,Melanie Königshoff,Aö Yildirim,Oliver Eickelberg +5 more
TL;DR: It is shown that lung function decline is not a prerequisite for histologically evident fibrosis, particularly during the onset or resolution thereof, and may thus be considered for the assessment of intraindividual therapeutic studies in preclinical studies of pulmonary fibrosis.
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The importance of detailed epigenomic profiling of different cell types within organs.
TL;DR: The lung is used to illustrate the importance of investigating an organ's purified cell epigenomes, and the challenges and promise of realizing a comprehensive catalog of primary cell epigenites are outlined.
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Mitochondrial 8-oxoguanine DNA glycosylase mitigates alveolar epithelial cell PINK1 deficiency, mitochondrial DNA damage, apoptosis, and lung fibrosis.
Seok Jo Kim,Seok Jo Kim,Paul Cheresh,Paul Cheresh,R. Jablonski,R. Jablonski,Lyudmila I. Rachek,Anjana V. Yeldandi,Raul Piseaux-Aillon,Mark Ciesielski,Karen M. Ridge,Karen M. Ridge,Cara J. Gottardi,Anna P. Lam,Annie Pardo,Moisés Selman,Viswanathan Natarajan,David W. Kamp,David W. Kamp +18 more
TL;DR: It is suggested that mtOGG1 maintenance of AEC mtDNA is crucial for preventing PINK1 deficiency that promotes apoptosis and lung fibrosis and strategies aimed at preserving AT2 cell mtDNA integrity may be an innovative target.
Journal ArticleDOI
Induction of Stemlike Cells with Fibrogenic Properties by Carbon Nanotubes and Its Role in Fibrogenesis
Sudjit Luanpitpong,Liying Wang,Amruta Manke,Karen H. Martin,Amanda Gatesman Ammer,Vincent Castranova,Yong Yang,Yon Rojansakul +7 more
TL;DR: It is shown that carbon nanotubes induced fibroblastic nodule formation in primary human lung fibroblast cultures resembling the fibroBlastic foci in clinical fibrosis and promoted FSCs that are highly fibrogenic and a potential driving force of fibrogenesis.
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Telomerase Mutations in Families with Idiopathic Pulmonary Fibrosis
Mary Armanios,Julian J.-L. Chen,Joy D. Cogan,Jonathan K. Alder,Roxann G. Ingersoll,Cheryl Markin,William Lawson,William Lawson,Mingyi Xie,Irma Vulto,John A. Phillips,Peter M. Lansdorp,Carol W. Greider,James E. Loyd +13 more
TL;DR: In this paper, the authors found that mutations in the genes encoding telomerase components can appear as familial idiopathic pulmonary fibrosis, which is a rare hereditary disorder associated with premature death from aplastic anemia and lung fibrosis.
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