Low Activity of Transcription Factor Triggers Pulmonary Fibrosis
The research was conducted on mice model progression of pulmonary fibrosis was inhibited using drugs that are known to boost FoxO3 activity.
Scientists from the Max Planck Institute for Heart and Lung Research in Bad Nauheim have reported that that reduced activity of the transcription factor FoxO3 plays important role in the development of pulmonary fibrosis. Pulmonary fibrosis is characterizes by inability of an individual to absorb adequate oxygen. The former and active heavy smokers from the age of 50 are affected by this disease. According to Oxygen Therapy Market report published by Coherent Market Insights, oxygen therapy can be used to treat patients with pulmonary fibrosis, which can lower down the intensity of the disease as this disease is incurable.
Fibroblasts, connective tissue cells play key role in pulmonary fibrosis. These cells provide structure to the alveoli in the lungs and characteristic changes to these fibroblasts are observed during development of the disease. Myofibroblasts are the modified cells responsible for the changes in connective tissue structure. During disease progression air sacs increasingly degenerate resulting into damaged blood vessels in the lungs, which causes shortness of breath.
The researchers were focused on detection of factor responsible for fibroblast changes, which could a key for possible treatment. The team compared connective tissue cells from healthy individuals and patients with pulmonary fibrosis. “We noticed a transcription factor called FoxO3. Cells from patients with pulmonary fibrosis contained less of this protein than cells from healthy controls. The results were even clearer once we looked at FoxO3 activity – it was much lower in fibroblasts from patients with pulmonary fibrosis than in cells from healthy people,” explained Soni Pullamsetti, Research Group lead, Max Planck Institute for Heart and Lung Research.
Mice model with pulmonary fibrosis was found to have reduced FoxO3 activity. The effect was high genetically modified mice to lack FoxO3. Reactivating FoxO3 in patients with pulmonary fibrosis might offer a way of treating the disease as treating mice with pulmonary fibrosis with UCN-01 resulted in a reduction in symptoms and improved lung function.
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