The discovery increases scientists’ understanding of the mechanisms underlying bronchopulmonary dysplasia and IPF. It also raises the possibility of treating both disorders by targeting the signaling dysfunction.
Researchers published the study in The American Journal of Pathology. The title is “A Shared Pattern of β-Catenin Activation in Bronchopulmonary Dysplasia and Idiopathic Pulmonary Fibrosis,”
Bronchopulmonary dysplasia and IPF occur on opposite sides of the human spectrum. Bronchopulmonary dysplasia stems from premature newborns’ long-term use of respiratory support, while IPF commonly develops in a person’s 60s or later.
Although they have different causes, growing evidence suggests they share common drivers of disease. One is problems with lung repair processes.
To gain insight on this topic, researchers looked at lung tissue samples from preterm infants with and without bronchopulmonary dysplasia, and from adults with IPF or COPD, which is a non-scarring lung illness. The team focused on the Wnt signaling pathway’s ability to activate beta-catenin gene regulatory protein.
Scientists know that the Wnt and beta-catenin signaling pathway is critical to normal lung development. Previous studies suggested it could take part in the collagen accumulation and fibrotic processes seen in bronchopulmonary dysplasia and IPF.
Analysis of healthy lung tissue samples collected at different stages of development confirmed that Wnt and beta-catenin signaling is activated in the nucleus of cells early in life. But the activation diminished over time and was almost absent in adults’ lungs, the researchers’ laboratory studies showed.
The team found similar activation patterns in the lungs of those with bronchopulmonary dysplasia and IPF. Studies in mice confirmed the lab findings.
In contrast, the same beta-catenin activation patterns were not found in lung tissue samples of COPD patients. This demonstrated that not only is Wnt and beta-catenin activation shared by bronchopulmonary dysplasia and IPF, but is required for fibrotic diseases to progress.
“The association of specific modifications of beta-catenin during normal lung development and again in response to lung injury supports the widely held concept that repair of lung injury involves the recapitulation of developmental programs,” the researchers wrote.
The team believes that using drugs that could prevent these activation signals and restricting the drug delivery to “the alveolar spaces of the lung” could stop the fibrotic process in both diseases.
“Targeting the Wnt pathway in this way may provide a novel strategy to restore lung health after injury,” the researchers wrote.
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