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Alveolar epithelial and endothelial cell apoptosis in emphysema: What we know and what we need to know

Authors Mathieu C Morissette, Julie Parent, Julie Milot

Published 2 December 2008 Volume 2009:4 Pages 19—31

DOI https://doi.org/10.2147/COPD.S4432

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Mathieu C Morissette, Julie Parent, Julie Milot

Centre de Recherche de l’Hôpital Laval, Institut Universitaire de Cardiologie et de Pneumologie de l’Université Laval, Québec, Canada

Abstract: Emphysema is mainly caused by cigarette smoking and is characterized by the loss of alveolar integrity and an enlargement of the alveolar space. However, mechanisms involved in its development are not fully understood. Alveolar cell apoptosis has been previously investigated in the lung of emphysematous subjects as a potential contributor to the loss of alveolar cell and has been found abnormally elevated. Though, mechanisms involved in the increased alveolar apoptosis that occurs in emphysema have now become a prolific field of research. Those mechanisms are reviewed here with special focus on how they affect cell viability and how they may be implicated in emphysema. Moreover, we suggest a model that integrates all those mechanisms to explain the increased alveolar apoptosis observed in emphysema. This review also includes some reflections and suggestions on the research to come.

Keywords: emphysema, apoptosis, proteases, VEGF, oxidative stress, TRAIL, autoimmunity

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