Pulmonary fibrosis is a condition that is caused by scarring of the lungs which can lead to shortness of breath and other respiratory issues. Some cases of COVID-19 have lead to pulmonary fibrosis.
Unfortunately, not knowing exactly what starts the fibrosis has made finding a treatment difficult. Currently, there is no available treatment besides a lung transplant.
Researchers have been working to study the lung tissue of patients suffering from the condition to try to find a molecular target to treat it. As a part of this investigation, tissue from COVID-19 patients has been studied.
Mice models have shown that blocking MBD2, an epigenetic regulator, was able to protect the mice from further lung damage. This was administered via intratracheal inhalation.
Prior to these mice models, tissues of damaged lungs from patients with systemic sclerosis, SARS-CoV-2, and unknown causes were studied. The mice models were made by the administration of bleomycin.
The team found that in both the mice models and the tissue samples studied previously, the fibrosis was characterized by an overexpression of the MBD2 epigenetic regulator. This expression was specifically found in areas that had macrophages. Macrophages were already known to be involved in the development of fibrosis.
After this finding, the team tried to deplete the MBD2 gene within the macrophage. This lead to a reduction of the macrophages inside the lungs, ultimately protecting them from fibrosis.
Researchers are hopeful about this new potential therapy because MBD2 doesn’t impact the DNA methylation process. This means that it could be a safe treatment for patients.
Next steps will involve investigating the impact of changed MBD2 expression for other cells impacted by the pulmonary fibrosis in patients.
You can read more about this recent study here.