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Normal lung development needs self-eating
David Warburton, Saverio Bellusci
David Warburton, Saverio Bellusci
Published June 4, 2019
Citation Information: J Clin Invest. 2019;129(7):2658-2659. https://doi.org/10.1172/JCI129442.
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Commentary

Normal lung development needs self-eating

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Abstract

Autophagy is a Greek-derived concept that means “self-eating” and is increasingly recognized as an important regulator of homeostasis and disease. In this issue of the JCI, Yeganeh et al. report the important finding that intrinsic autophagy is required for normal progression of lung development. Conditional deletion of the beclin 1–encoding gene (Becn1) specifically within lung epithelial cells of embryonic mice resulted in neonatal lethal respiratory distress that was associated with negative impacts on airway branching and differentiation of airway epithelial cell lineages. The authors draw speculative parallels with the alveolar simplification phenotype of bronchopulmonary dysplasia in premature human infants and suggest that stimulation of autophagy by AMP-dependent kinase activation might conceivably rescue these phenotypes.

Authors

David Warburton, Saverio Bellusci

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