Fibrosis: From Basic Mechanisms to Targeted Therapies
joint with Stromal Cells in Immunity
Organizer(s): Robert Lafyatis, Paolo G.V. Martini, Dean Sheppard and Lucie PedutoDate: February 07 - 11, 2016
Location: Keystone Resort, Keystone, CO, USA
Fibrosis is the primary process of many diseases and the end-stage of many more, frequently leading to organ failure. However, the mechanisms leading to fibrosis have been poorly understood and available therapeutics targeting fibrosis limited. Increasingly, fibrosis is understood as a dynamic process that is orchestrated by the immune system, or activated by inflammation or cellular stress. Fibrosis of lung, kidney, skin, liver and muscle typically follow a variety of different stimuli. Advances in understanding Th2 cell responses, cell death, the inflammasome and ER and oxidative stresses provide new insights into such stimuli. Understanding the regulation of and interaction between profibrotic cytokines such as TGFb, IL-13, and CTGF are shedding additional light on fibrotic processes. Recent studies indicate that fibrosis is mediated by dedicated progenitor and resident cells within target tissues. Fibroblast and perivascular cell phenotype and differentiation are regulated not only by cytokines, but also by matrix composition and stiffness. Advances in the treatment of idiopathic pulmonary fibrosis and systemic sclerosis herald many new anti-fibrotic therapies that will soon enter clinical trials. Thus, mechanistic understandings will soon answer the long-standing clinical challenges of fibrotic and end-stage scarring diseases. This meeting aims to: 1) Present and discuss the most current and cutting-edge results regarding the mechanisms, signaling pathways, gene regulation, cells and tissues involved in fibrotic diseases and therapeutic approaches currently in development; 2) Include discussions and presentation of new ideas or paradigms that challenge existing models and expand on the knowledge of the current standard of care for fibrotic diseases; 3) Consider the future directions of the field, including the identification of the most pressing unanswered questions, the areas needing more focus, and those that would benefit from new approaches and methodologies developed and used in other related fields; 4) Stimulate collaborations in a setting conducive to focused, intense discussion among scientists with broad interests in fibrotic diseases and different targeted therapeutic approaches, including engagement with industrial partners interested in new targets in fibrotic disease; and 5) Provide a forum for trainees and new investigators to learn about current work in the field, to present their own work and to network with established investigators.
Scholarship Deadline: October 8 2015
Discounted Abstract Deadline: October 8 2015
Abstract Deadline: November 10 2015
Discounted Registration Deadline: December 8 2015
We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:
Gilead Sciences, Inc.
We gratefully acknowledge the generous grant for this conference provided by:National Heart, Lung, and Blood Institute (NHLBI)
Grant No. 1R13HL131040-01
Funding for this conference was made possible (in part) by 1R13HL131040-01 from the National Institutes of Health. The views expressed in written conference materials or publications and by speakers and moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention of trade names, commercial practices, or organizations imply endorsement by the U.S. Government.