Abstract
The excessive activation of the Wnt/β-catenin signaling pathway is an important regulatory mechanism that underlies the excessive proliferation and impaired differentiation of type 2 alveolar epithelial cells (AEC-II) in bronchopulmonary dysplasia (BPD). Sox9 has been shown to be an important repressor of the Wnt/β-catenin signaling pathway and plays an important regulatory role in various pathophysiological processes. We found that the increased expression of Sox9 in the early stages of BPD could downregulate the expression of β-catenin and promote the differentiation of AEC-II cells into AEC-I, thereby alleviating the pathological changes in BPD. The expression of Sox9 in BPD is regulated by long noncoding RNA growth arrest-specific 5. These findings may provide new targets for the early intervention of BPD.
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