Medical Summary
Nico Nunez
Medical Terminology
Mrs. Rivera
26 April 2013
Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases
Fibrosis is often defined as a wound-healing response chat has gone out of control. Stimulated epithelial cells, endothelial cells, and myofibroblasts also produce MMPs, which disrupt the basement membrane, and additional cytokines and chemokine’s that recruit and activate neutrophils, macrophages, T cells, B cells, and eosinophil’s, important components of reparative tissue. Despite having obvious ecological and clinical distinctions, most chronic fibrotic disorders have in common a persistent irritant that sustains the production of growth factors, proteolytic enzymes, angiogenic factors, and fibrogenic cytokines, which together stimulate the deposition of connective tissue elements that progressively remodel and destroy normal tissue architecture (1,2). Collagen fibers also become more organized, blood vessels are restored to normal, scar tissue is eliminated, and epithelial and/or endothelial cells divide and migrate over the basal layers to regenerate the epithelium or endothelium, respectively, restoring the damaged tissue to its normal appearance. Persistent inflammation, tissue necrosis, and infection lead to chronic myofibroblast activation and excessive accumulation of ECM components, which promotes the formation of a permanent fibrotic scar. In contrast to acute inflammatory reactions, which are characterized by rapidly resolving vascular changes, edema, and neutrophilic infiltration, pathogenic fibrosis typically results from chronic inflammatory reactions - defined as responses that persist for several weeks or months and in which inflammation, tissue destruction, and repair processes occur simultaneously. Because fibrocytes produce various factors that are involved in mediating fibro proliferation (6), interrupting critical chemokine signaling pathways could impact the pathogenesis of pulmonary fibro
Medical Terminology
Mrs. Rivera
26 April 2013
Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases
Fibrosis is often defined as a wound-healing response chat has gone out of control. Stimulated epithelial cells, endothelial cells, and myofibroblasts also produce MMPs, which disrupt the basement membrane, and additional cytokines and chemokine’s that recruit and activate neutrophils, macrophages, T cells, B cells, and eosinophil’s, important components of reparative tissue. Despite having obvious ecological and clinical distinctions, most chronic fibrotic disorders have in common a persistent irritant that sustains the production of growth factors, proteolytic enzymes, angiogenic factors, and fibrogenic cytokines, which together stimulate the deposition of connective tissue elements that progressively remodel and destroy normal tissue architecture (1,2). Collagen fibers also become more organized, blood vessels are restored to normal, scar tissue is eliminated, and epithelial and/or endothelial cells divide and migrate over the basal layers to regenerate the epithelium or endothelium, respectively, restoring the damaged tissue to its normal appearance. Persistent inflammation, tissue necrosis, and infection lead to chronic myofibroblast activation and excessive accumulation of ECM components, which promotes the formation of a permanent fibrotic scar. In contrast to acute inflammatory reactions, which are characterized by rapidly resolving vascular changes, edema, and neutrophilic infiltration, pathogenic fibrosis typically results from chronic inflammatory reactions - defined as responses that persist for several weeks or months and in which inflammation, tissue destruction, and repair processes occur simultaneously. Because fibrocytes produce various factors that are involved in mediating fibro proliferation (6), interrupting critical chemokine signaling pathways could impact the pathogenesis of pulmonary fibro