Pulmonary fibrosis: pathogenesis, etiology and regulation
By M. Wilson, TA Wynn. Mucosal Immunology, 2009
804 citations recorded by the source corpus.
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.
Subfields: Public Health, Environmental and Occupational Health, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/5c0a15de219764cf312980941b85e2f1c5e4cc7b
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In Pulmonary and Respiratory Medicine
Citations in the corpus
- Bleomycin and IL-1β–mediated pulmonary fibrosis is IL-17A dependent (2010, background): “20092121 535 Despite distinct etiological and clinical features, most chronic fibrotic disorders have in common a persistent irritant that sustains the production of growth factors, proteolytic enzymes, angiogenic factors, and fibrogenic cytokines (Wilson and Wynn, 2009).”
- Alternative activation of macrophages: mechanism and functions. (2010, background): “Induction of Arg1 by IL-4 and IL-13 has been implicated in collagen deposition (Hesse et al., 2001) and degradation (reviewed in Wilson and Wynn, 2009).”