Researchers seek to reverse lung injury caused by cancer treatments.
A recent study has discovered that a transcription factor, FOXF1, activates biological processes that stimulates lung repair after an injury.
Two laboratories are now developing a pharmacologic compound that stimulates FOXF1, which generated lung repair in mouse models, according to a study published in Science Signaling.
"Besides toxic insults from some cancer treatments, acute lung injury can be a major medical problem for people who get infectious diseases like flu, pneumonia or Ebola because of pathogens that target the lung," said Vladimir Kalinichenko, MD, PhD, co-senior author of the study. "A small molecule compound we developed efficiently stabilizes the FOXF1 protein in cell cultures and mouse lungs, and it shows promise in inhibiting lung inflammation and protecting experimental mice from lung injury."
Through the study, researchers found that mice died of respiratory problems when there was a loss of FOXF1 in lung endothelial cells.
According to the study, mutations in the FOXF1 gene can cause alveolar capillary dysplasia, a fatal congenital lung disorder. Researchers state that this condition shows the importance of FOXF1 in the respiratory system.
Researchers suggest that stabilizing or restoring FOXF1 will increase blood vessel formation in the lungs, increase healing, and decrease breathing complications.
Investigators are conducting a follow up of this study to develop the targeted small molecule and are determining safety and efficacy in mouse models.
According to the study, additional research is needed before this compound will be tested in humans.