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Fibrosis: From Basic Mechanisms to Targeted Therapies

纤维化：从基本机制到靶向治疗

基本信息

批准号：
9039836
负责人：
DAVID L. WOODLAND
金额：
$ 1.5万
依托单位：
KEYSTONE SYMPOSIA
依托单位国家：
美国
项目类别：
财政年份：
2016
资助国家：
美国
起止时间：
2016-02-01 至 2017-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9039836
关键词：
Address Adult Affect Alcohols Animal Disease Models Area Biology Burn injury Cell Death Cells Cellular Stress Child Chronic Disease Chronic Kidney Failure Cicatrix Cirrhosis Clinical Clinical Trials Collaborations Colorado Complication Contracture Crohn&apos s disease Development Diagnosis Disease Event Fibroblasts Fibrosis Functional disorder Future Gene Expression Regulation Hamman-Rich syndrome Healed Health Heart failure High Prevalence Immune system Inflammation Interleukin-13 Interstitial Lung Diseases Intestines Joints Kidney Kidney Diseases Kidney Failure Knowledge Learning Life Light Liver Liver diseases Lung diseases Mediating Medical Methodology Mission Modality Modeling Morbidity - disease rate Muscle Muscular Dystrophies Myocardial Infarction National Heart, Lung, and Blood Institute Organ Organ failure Outcome Oxidative Stress Patients Pericytes Pharmacologic Substance Phenotype Prevalence Process Public Health Pulmonary Fibrosis Regulation Renal Glycosuria Research Research Personnel Scientist Signaling Protein Skin Speed Staging Stimulus Systemic Lupus Erythematosus Systemic Scleroderma Th2 Cells Therapeutic Therapeutic Intervention Time Tissues Translations Viral Work clinical application clinical practice connective tissue growth factor cytokine end stage disease healing insight interest meetings new technology nonalcoholic steatohepatitis novel strategies novel therapeutics posters progenitor response standard of care symposium targeted treatment therapeutic target

项目摘要

DESCRIPTION (provided by applicant): Support is requested for a Keystone Symposia meeting entitled Fibrosis: From Basic Mechanisms to Targeted Therapies, organized by Robert Lafyatis, Paolo G.V. Martini, Dean Sheppard and Lucie Peduto. The meeting will be held in Keystone, Colorado from February 7-11, 2016. 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 differentiatio 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. Thus, this meeting addresses an important public health challenge relevant to the NHLBI mission. Specifically, fibrosis is the end stage and life-threatening complication of most interstitial lung diseases, affecting many adults and children. Current treatments for fibrotic lun disease are extremely limited, so it continues to represent a major national health problem. The most common form of pulmonary fibrosis, Idiopathic Pulmonary Fibrosis (IPF), has a prevalence in the US of between 28 and 63/100,000 depending on whether narrow or more broad criteria are used for case definition. Current estimates are that the mean survival is 3 years from the time of diagnosis. The prevalence of pulmonary fibrosis from all causes is probably 3 times higher than the prevalence of IPF.