Apoptosis plays an important role in normal lung development as well as repair after lung injury and contributes to the pathophysiology of many lung diseases. Bronchopulmonary dysplasia (BPD) is a major cause of neonatal pulmonary and non-pulmonary morbidity and is characterized by an arrest in alveolar development. Currently there is no specific treatment for BPD. Mechanical ventilation, exposure to high concentrations of oxygen and inflammation are important risk factors for the development of BPD. Emerging evidence links the pathophysiology of BPD to an imbalance between anti-apoptotic and pro-apoptotic signaling pathways. Different apoptotic signaling pathways have been implicated, including Fas/FasL, caspase-dependent and -independent pathways, pro-survival Akt, transforming growth factor-β and p53. To what extent these pathways are involved in the pathogenesis of BPD is a hot topic of research. The aim of this review is to describe the timing and apoptotic events during lung development and the pathogenesis of BPD with particular focus upon apoptotic pathways activated by mechanical ventilation, hyperoxia and inflammation. An appreciation of these apoptotic pathways is essential for understanding the aetiology of and the development of treatments for pulmonary diseases such as BPD.
Keywords: Cell death, inflammation, lung, oxidative stress, ventilation, dysplasia, apoptosis, Bronchopulmonary, Signaling
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