The Enigma Variations: The Many Faces of the Myofibroblast in Fibrotic Disease
Sponsored by: Respiration Section
Track: Tissue Remodeling and Repair
Monday, April 28, 2014
3:15 PM – 5:15 PM
Room 28B, San Diego Convention Center
Rachel C. Chambers
Paul F. Mercer
There is currently a paucity of pharmacological interventions for fibrotic disorders of the lung, which account for significant levels of mortality akin to many forms of cancer. The development of pulmonary fibrosis is thought be driven by a dysregulated wound healing response, through continual local injury or impaired control mechanisms. Uncontrolled or sustained activation of mesenchymal cell populations leads to differentiation of fibroblasts into contractile myofibroblasts, excessive deposition of extracellular matrix proteins, gross tissue distortion and eventually can lead to complete loss of organ function. Despite being widely accepted as the central effector cell in fibrosis affecting all organs, our understanding of the myofibroblast and its contribution to fibrotic pathology has only begun to develop relatively recently. Critical questions including the origin of the myofibroblast, understanding fibroblast heterogeneity and in addition to how the myofibroblast responds and contributes to the fibrotic milieu, all remain largely unresolved.
This symposium is aimed at basic and translational scientists engaged in understanding fibrotic cell biology on the lung and prosecuting therapeutic targets in this area. It will bring together world class researchers focussing on a range of aspects of myofibroblast biology including progenitor tracing, the response of myofibroblasts to environmental ques, and myofibroblast metabolism during disease. The aim of the symposium will be to establish critical pathways in myofibroblast biology pertinent to lung fibrosis by drawing on world class researchers, investigating myofibroblast cell biology in a variety of settings. The attendee will come away with an understanding of the processes central to myofibroblast cell biology in fibrosis and will have a good grasp of the key questions which still require resolution in this field. It is hoped that this arena could serve as a seed for potential cross collaboration between researchers interested in fibrotic cell biology in a range of different organ systems.
Who are you and where do you come from? The origin of the myofibroblast.
Jeremy Duffield. Univ. of Washington
The stressed out myofibroblast: thriving under tension.
Boris Hinz. Univ. of Toronto
PI3 kinase: An oncogenic target in fibrosis.
Paul F Mercer. Univ. College London
Where do we go from here? Emerging myofibroblast targets in lung fibrosis.
Patricia J. Sime. Univ. of Rochester Med. Ctr.