AI Article Synopsis
- * Research using mouse models reveals that alveolar type 1 (AT1) cells can transform into alveolar type 2 (AT2) cells following lung injury, which aids in lung recovery during early postnatal development.
- * Hippo signaling plays a crucial role in this cellular plasticity, highlighting a new understanding of how lung tissue can regenerate, particularly during different developmental stages.
Article Abstract
Regeneration of the architecturally complex alveolar niche of the lung requires precise temporal and spatial control of epithelial cell behavior. Injury can lead to a permanent reduction in gas exchange surface area and respiratory function. Using mouse models, we show that alveolar type 1 (AT1) cell plasticity is a major and unappreciated mechanism that drives regeneration, beginning in the early postnatal period during alveolar maturation. Upon acute neonatal lung injury, AT1 cells reprogram into alveolar type 2 (AT2) cells, promoting alveolar regeneration. In contrast, the ability of AT2 cells to regenerate AT1 cells is restricted to the mature lung. Unbiased genomic assessment reveals that this previously unappreciated level of plasticity is governed by the preferential activity of Hippo signaling in the AT1 cell lineage. Thus, cellular plasticity is a temporally acquired trait of the alveolar epithelium and presents an alternative mode of tissue regeneration in the postnatal lung.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8500919 | PMC |
| http://dx.doi.org/10.1016/j.stem.2021.04.026 | DOI Listing |
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