Abstract
In 1972, Kerr and Currie described a new type of cell death characterized by morphological changes distinct from the features observed during necrosis (1). The term of “apoptosis” was adopted to describe this highly conserved genetic program leading to regulated cellular self-destruction. Subsequent investigations showed that this programmed cell death is crucial during fetal development and critical for controlling harmful mechanisms triggered by environmental stresses. Recent literature has defined new roles for apoptosis in the normal and injured lung. For example, apoptosis plays an important role in postnatal lung development (2), and it is evident that resolution of lung inflammation after bacterial infection occurs by neutrophil apoptosis (3). While there is an increasing body of evidence supporting a role for apoptosis in the remodeling of the lung after acute lung injury (ALI) (3, 4), the factors that regulate normal and abnormal apoptotic cell death during ALI remain to be fully elucidated.
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Faure, K., Guery, B., Pittet, J.F. (2001). Apoptosis in Acute Lung Injury. In: Wong, H.R., Shanley, T.P. (eds) Molecular Biology of Acute Lung Injury. Molecular and Cellular Biology of Critical Care Medicine, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1427-5_15
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DOI: https://doi.org/10.1007/978-1-4615-1427-5_15
Publisher Name: Springer, Boston, MA
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