Mechanisms of pulmonary fibrosis.

By V. Thannickal, G. Toews, E. White, J. Lynch, F. Martinez. Annual Review of Medicine, 2004

792 citations recorded by the source corpus.

Subfields: Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/cac9f0d0fc08d7a77c79a3f50096f31c19c282ec

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Pulmonary and Respiratory Medicine

1. B. Hinz
2. TA Wynn
3. V. Thannickal
4. W. Macnee
5. Nikolaos G. Frangogiannis
6. D. Parums

Citations in the corpus

• NADPH Oxidase-4 Mediates Myofibroblast Activation and Fibrogenic Responses to Lung Injury (2009, background): “2005" language="eng" relation="no"> Tissue repair in mammals involves the integrated actions of growth factors and matrix molecules that orchestrate cell-to-cell interaction”
• Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix (2007, positive): “However, the evolution of pulmonary fi brosis toward end-stage fi brotic lung disease depends on the persistence of αvβ6-negative Mfs to express and activate latent TGF-β1 (Phan, 2002; Thannickal et al., 2004).”
• Standardized quantification of pulmonary fibrosis in histological samples. (2008, background): “Correlation analysis between biochemical parameter and histopathological scales may be interesting, however, it may be less useful comparing the extent of fibrosis in different lobes/lungs, as the bleomycin model is highly variable in the extent of fibrosis (3,8,12).”
• High-dose acetylcysteine in idiopathic pulmonary fibrosis. (2005, background): “Blood lactate dehydrogenase increased 6 6 (8) 2 2 (3)”
• Reversal of Persistent Fibrosis in Aging by Targeting Nox4-Nrf2 Redox Imbalance (2014, background): “The inability to terminate the host reparative response, specificallymyofibroblast activation/accumulation, may underlie the progressive nature of fibrotic reactions in injured tissues (7).”
• Cellular and molecular mechanisms of fibrosis (2008, neutral): “help slow the progression of fibrosis [8,171,172].”
• miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis (2010, background): “Uncontrolled ECM production can lead to clinically important fibrotic diseases, including idiopathic pulmonary fibrosis (IPF) (Tomasek et al., 2002; Thannickal et al., 2004).”
• Formation and function of the myofibroblast during tissue repair. (2007, background): “Myofibroblast-generated contractures are also characteristic for fibrosis affecting vital organs such as the liver (Desmouliere et al., 2003), heart (Virag and Murry, 2003; Brown et al., 2005), lung (Phan, 2002; Thannickal et al., 2004), and kidney (Lan, 2003).”
• Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “The fate of myofibroblasts, regardless of their origin(s), in injured tissues may ultimately determine whether normal healing occurs or whether progression to end-stage fibrosis ensues.(121,126) There is likely to be significant heterogeneity in lung fibroblasts, including anti-fibrotic subpopulatio”
• The myofibroblast: paradigm for a mechanically active cell. (2010, background): “, 2005), lung (Phan, 2002; Thannickal et al., 2004) and kidney (Liu,”
• Integrating mechanisms of pulmonary fibrosis (2011, background): “Although some types of pulmonary fibrosis maintain a significant inflammatory component throughout the course of the disease, other forms like IPF are often characterized as exhibiting highly progressive fibrotic disease in the absence of detectable inflammation (Thannickal et al., 2004).”