STAT3: A central mediator of pulmonary fibrosis?

Cecilia Prele, Eric Yao, Robert J. J. O'Donoghue, Steven E. Mutsaers, Darryl A. Knight

Research output: Chapter in Book/Conference paperConference paperpeer-review

40 Citations (Scopus)


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 ordefective 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 profibrotic processes. An improved understanding of the complex celltype specific roles that this transcription factor plays in normal lung and in fibrosis is required to determine its suitability as an effective therapeutic target.

Original languageEnglish
Title of host publicationProceedings of the American Thoracic Society
EditorsGeoffrey J. Laurent
Place of PublicationUnited States
PublisherAmerican Thoracic Society
Number of pages6
ISBN (Print)1546-3222
Publication statusPublished - 15 Jul 2012
Event27th Transatlantic Airway Conference - Lucerne, Switzerland
Duration: 19 Jan 201220 Jan 2012


Conference27th Transatlantic Airway Conference


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