Current concepts suggest that COPD largely results from tissue injury, most commonly consequent to an exposure, the most important of which is cigarette smoke. This injury is mediated by a complex network of inflammatory cells and mediators, and it is likely that heterogeneity in the inflammatory response accounts for some of the variable susceptibility to develop COPD and for the some of the clinical heterogeneity of the disease. Mechanisms that can prevent tissue injury are also diverse and are inhibited to varying degrees among individuals with COPD. Finally, the alterations in tissue structure that compromise function depend not only on tissue injury, but also on tissue repair,which can either mitigate or exacerbate lung function loss depending on whether repair processes are effective or disruptive.
|Original language||English (US)|
|Number of pages||7|
|Journal||Pneumonologia i Alergologia Polska|
|State||Published - Mar 11 2011|
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