It has been established that airway inflammatory processes are pivotal as the pathological features of bronchial asthma. Standard therapy with inhaled corticosteroids markedly suppresses such inflammatory changes, resulting in clinical beneficial effects. However, it is now clear that several histological changes including goblet cell hyperplasia, sub-epithelial collagen deposits, increased capillary networks and smooth muscle hypertrophy occur as a chronic consequence of this airway disorder even by the recommended strategies with steroid treatment. These pathologic changes, so-called remodeling, play an important role in the increased airway obstruction and hyperresponsiveness, and eventually in the development of irreversible respiratory failure. Recent studies have elucidated that myofibroblasts and smooth muscle cells play a vital role in these processes. Therefore, agents regulating proliferation and differentiation of these cells may become new therapeutic strategies for the near future.
Keywords: lung fibroblast, myofibroblast, smooth muscle actin, smotth muscle cells, cytokines, chemokines, growth factor
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