Apoptosis in lung injury and fibrosis.
Pulmonary fibrosis is characterised by fibroblast accumulation and alveolar epithelium denudation. Increased apoptosis of alveolar epithelial cells and decreased apoptosis of fibroblasts may play an important role in the pathogenesis of disease. Inflammatory cells can modulate apoptosis of other cell types, both by removal of apoptotic debris and by cytokine production, thus preserving a pro-fibrotic environment. In the present review, some of the mechanisms by which apoptosis may contribute to the pathogenesis of idiopathic pulmonary fibrosis are described.
Drakopanagiotakis
F
F
Interstitial Lung Disease Study Group, 3rd Dept of Pneumonology, Sismanoglio General Hospital, Athens, Greece.
Xifteri
A
A
Polychronopoulos
V
V
Bouros
D
D
D000375:Aging; D017209:Apoptosis; D004247:DNA / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D000860:Hypoxia; D007249:Inflammation; D055370:Lung Injury / Q000473:pathology*; D008264:Macrophages / Q000378:metabolism; D008954:Models, Biological; D009504:Neutrophils / Q000378:metabolism; D011658:Pulmonary Fibrosis / Q000473:pathology*; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D004247:DNA