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Current thinking suggests that idiopathic pulmonary fibrosis (IPF) is initiated by pathways similar to normal wound healing, but relentless fibrosis occurs secondary to absent or defective inhibitory mechanisms that normally terminate wound healing. The heterogeneous pathological presentation of fibrosis suggests that the anatomic location and origin of fibroblasts and other cells might be critical for their phenotype and function and will impact on strategies to prevent or treat fibrotic lung diseases. This review summarizes our current understanding of the pathobiology of IPF, with a specific focus on the role of STAT3 in regulating cellular responses that may contribute to or inhibit pro-fibrotic processes. An improved understanding of the complex cell-type specific roles that this transcription factor plays in normal lung and in fibrosis is required to determine its suitability as an effective therapeutic target.<\/jats:p>","DOI":"10.1513\/pats.201201-007aw","type":"journal-article","created":{"date-parts":[[2012,7,16]],"date-time":"2012-07-16T06:28:51Z","timestamp":1342420131000},"page":"177-182","source":"Crossref","is-referenced-by-count":51,"title":["STAT3: A Central Mediator of Pulmonary Fibrosis?"],"prefix":"10.1093","volume":"9","author":[{"given":"Cecilia M.","family":"Pr\u00eale","sequence":"first","affiliation":[{"name":"Lung Institute of Western Australia and Centre for Asthma, Allergy, and Respiratory Research, School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric","family":"Yao","sequence":"additional","affiliation":[{"name":"University of British Columbia James Hogg Research Centre, Vancouver, British Columbia, Canada"},{"name":"Department of Anesthesiology, Pharmacology, and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert J. 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