The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Pulmonary fibrosis: pathogenesis, etiology and regulation
Open accessAbstract
Pulmonary fibrosis and architectural remodeling of tissues can severely disrupt lung function, often with fatal consequences. The etiology of pulmonary fibrotic diseases is varied, with an array of triggers including allergens, chemicals, radiation and environmental particles. However, the cause of one of the most common pulmonary fibrotic conditions, idiopathic pulmonary fibrosis (IPF), is still unclear. This review examines common mechanisms of pulmonary wound-healing responses following lung injury, and highlights the pathogenesis of some of the most widespread pulmonary fibrotic diseases. A three phase model of wound repair is reviewed that includes; (1) injury; (2) inflammation; and (3) repair. In most pulmonary fibrotic conditions dysregulation at one or more of these phases has been reported. Chronic inflammation can lead to an imbalance in the production of chemokines, cytokines, growth factors, and disrupt cellular recruitment. These changes coupled with excessive pro-fibrotic IL-13 and/or TGFβ1 production can turn a well-controlled healing response into a pathogenic fibrotic response. Endogenous regulatory mechanisms are discussed including novel areas of therapeutic intervention. Restoring homeostasis to these dysregulated healing responses, or simply neutralizing the key pro-fibrotic mediators may prevent or slow the progression of pulmonary fibrosis.
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Cites
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Interleukin-10 and the Interleukin-10 Receptor
Moore, K. W., de Waal Malefyt, R., Coffman, R. L., & O'Garra, A. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.683 · Cited by 6,737
Myofibroblasts and mechano-regulation of connective tissue remodelling
Tomasek, J. J., Gabbiani, G., Hinz, B., Chaponnier, C., & Brown, R. A. (2002) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm809 · Cited by 4,290
Fibrotic disease and the TH1/TH2 paradigm
Wynn, T. A. (2004) · Nature Reviews Immunology · doi:10.1038/nri1412 · Cited by 1,765
Self-citationEder, W., Ege, M. J., & von Mutius, E. (2006) · New England Journal of Medicine · doi:10.1056/nejmra054308 · Cited by 1,621
Peripheral Blood Fibrocytes: Differentiation Pathway and Migration to Wound Sites
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Metalloproteinases and their inhibitors: Regulators of wound healing
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Self-citationIL-13 Activates a Mechanism of Tissue Fibrosis That Is Completely TGF-β Independent
Kaviratne, M., Hesse, M., Leusink, M., Cheever, A. W., Davies, S. J., McKerrow, J. H., Wakefield, L. M., Letterio, J. J., & Wynn, T. A. (2004) · The Journal of Immunology · doi:10.4049/jimmunol.173.6.4020 · Cited by 370
Self-citation
Cited by
Alternative activation of macrophages: mechanism and functions
Gordon, S., & Martinez, F. O. (2010) · Immunity · doi:10.1016/j.immuni.2010.05.007 · Cited by 4,197
Nathan, C., & Ding, A. (2010) · Cell · doi:10.1016/j.cell.2010.02.029 · Cited by 2,183
Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus
Monticelli (2011) · PubMed · doi:10.1031/ni.2131 · Cited by 1,286
Bleomycin and IL-1β–mediated pulmonary fibrosis is IL-17A dependent
Wilson, M. S., Madala, S. K., Ramalingam, T. R., Gochuico, B. R., Rosas, I. O., Cheever, A. W., & Wynn, T. A. (2010) · Journal of Experimental Medicine · doi:10.1084/jem.20092121 · Cited by 730
Self-citationAcellular Normal and Fibrotic Human Lung Matrices as a Culture System for In Vitro Investigation
Booth, A. J., Hadley, R., Cornett, A. M., Dreffs, A. A., Matthes, S. A., Tsui, J. L., Weiss, K., Horowitz, J. C., Fiore, V. F., Barker, T. H., et al. (2012) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201204-0754oc · Cited by 665
Metadata
- Authors
- Wilson, M. S., & Wynn, T. A.
- Venue
- Mucosal Immunology
- Publisher
- Elsevier BV
- Published
- 2009-03
- Volume
- 2
- Issue
- 2
- Pages
- 103-121
- ISSN
- 1933-0219 (ISSN-L)
- OpenAlex
- W2064307892
- Cited by
- 822
- References
- 17
- FWCI
- 31.76
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
