Normal lung development needs self-eating
David Warburton1 and Saverio Bellusci1,2
1The Saban Research Institute, Children’s Hospital Los Angeles, USC, Los Angeles, California, USA.
2Justus Liebig University, Giessen, Germany.
Address correspondence to: David Warburton, Children’s Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 91011, USA. Phone: 323.361.5422; Email: dwarburton@chla.usc.edu.
Find articles by Warburton, D. in: JCI | PubMed | Google Scholar
1The Saban Research Institute, Children’s Hospital Los Angeles, USC, Los Angeles, California, USA.
2Justus Liebig University, Giessen, Germany.
Address correspondence to: David Warburton, Children’s Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 91011, USA. Phone: 323.361.5422; Email: dwarburton@chla.usc.edu.
Find articles by Bellusci, S. in: JCI | PubMed | Google Scholar
First published June 4, 2019 - More info
J Clin Invest. 2019;129(7):2658–2659. https://doi.org/10.1172/JCI129442.
© 2019 American Society for Clinical Investigation
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.
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Copyright © 2019 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)