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STAT3: A central mediator of pulmonary fibrosis?

Prêle, C.M., Yao, E., O’Donoghue, R.J.J., Mutsaers, S.E. and Knight, D.A. (2012) STAT3: A central mediator of pulmonary fibrosis? Proceedings of the American Thoracic Society, 9 (3). pp. 177-182.

Link to Published Version: https://doi.org/10.1513/pats.201201-007AW
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Abstract

Pulmonary fibrosis is a devastating, relentlessly progressive, and lethal disease. There is a significant unmet need for effective treatment since currently no FDA-approved therapies exist. 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.

Item Type: Journal Article
Publisher: American Thoracic Society
Copyright: © 2012 American Thoracic Society
URI: http://researchrepository.murdoch.edu.au/id/eprint/64357
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