Idiopathic pulmonary fibrosis at a molecular level
The cause of Idiopathic Pulmonary Fibrosis (IPF) is unknown but it is widely accepted that repeated injury to the epithelium leads to dysregulated healing, initiating a cascade of processes resulting in ﬁbroblast / myoﬁbroblast accumulation and overproduction and deposition of collagen.
Researchers at the Institute for Respiratory Health have pioneered studies identifying the gp130-induced signal transducer and activator of transcription (STAT)3 signalling pathway as pivotal in the development of lung ﬁbrosis.
What regulates STAT3-mediate ﬁbrosis is not clear but their current studies are focussing on understanding the role of mediators known to activate the pathway, cell types that may be regulating the mediator response, as well as a possible breakdown in regulation of the naturally occurring inhibitors that normally control the STAT3 response.
To get involved or for more information, contact the Research Leader.
A/Prof Cecilia Prêle
BSc (Hons), PhD
Head of Tissue Repair Group