Browsing by Subject "Collagenase"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    Open Access
    Liver fibrosis, the hepatic stellate cell and tissue inhibitors of metalloproteinases
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2000) McCrudden, R.; Iredale, J. P.
    Liver fibrosis occurs as a consequence of net accumulation of matrix proteins (especially collagen types I and III) in response to liver injury. The pathogenesis of liver fibrosis is underpinned by the activation of hepatic stellate cells (HSC) to a myofibroblast like phenotype with a consequent increase in their synthesis of matrix proteins such as interstitial collagens that characterise fibrosis. In addition to this there is increasing evidence that liver fibrosis is a dynamic pathologic process in which altered matrix degradation may also playa major role. Extracellular degradation of matrix proteins is regulated by matrix metalloproteinases (MMPS) - produced by HSC - which in turn are regulated by several mechanisms which include regulation at the level of the gene (transcription and proenzyme synthesis), cleavage of the proenzyme to an active form and specific inhibition of activated forms by tissue inhibitors of metalloproteinases (TIMPS). Insights gained into the molecular regulation of HSC activation will lead to therapeutic approaches in treatment of hepatic fibrosis in the future , and could lead to reduced morbidity and mortality in patients with chronic liver injury .
  • Thumbnail Image
    Publication
    Open Access
    Proteinase-antiproteinase imbalance in the pathogenesis of Emphysema: The role of metalloproteinases in lung damage
    (Murcia : F. Hernández, 1999) Pardo, A.; Selman, M.
    Pulmonary emphysema refers to a lung disorder characterized by a diffuse destruction of the alveolar walls resulting in enlargement of the distal airspaces. The disease is usually a chronic, progressive, and disabling disorder. The concept of proteinaselantiproteinase imbalance evolved from the identification of patients with al-antytripsin deficiency, and from the development of experimental emphysematous lesions using different enzymes. For a long time, this concept was seen as an elastase/antielastase imbalance, with the consequent degradation of elastin. Recent evidence, however, suggests that an intricate process of pulmonary remodeling occurs during the development of emphysema, where a complex network of serine proteases and metalloproteinases capable of degrading different extracellular matrix molecules, primarily, but not exclusively fibrillar collagens and elastin, are implicated in the pathogenesis of this disease.