Many breakthrough stories have surfaced, linking coronavirus with other diseases, as Covid-19 continues to affect millions worldwide.
A study has been recently published in the journal Science Advances that analyzed lung tissues from patients with different types of pulmonary fibrosis from Covid-19 patients. The study has revealed a promising molecular target to improve the chronic and irreversible disease.
Pulmonary fibrosis is a lung disease that happens when lung tissues gets damaged and scarred. This makes it harder for the lung to work properly. The symptoms of the disease are shortness of breath, a dry cough, feeling tired, and weight loss.
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Experiments in mouse models of lung fibrosis showed that administering blockers of an epigenetic regulator called MBD2 via intratracheal inhalation protected the mice against fibrotic lung injury, highlighting a potentially viable therapy.
The lack of understanding of what causes pulmonary fibrosis has greatly delayed the development of treatments. Therefore, no effective therapy is available other than lung transplantation in this case.
The researchers from Shenzhen University in China studied lung samples from patients with pulmonary fibrosis triggered by one of three causes: SARS-CoV-2 infection, systemic sclerosis-associated interstitial lung disease, or an unknown factor.
The researchers also studied mouse models of pulmonary fibrosis, which they induced in the animals by administering the compound bleomycin. They found, all cases of pulmonary fibrosis were characterized by overexpression of MBD2.
This activity was restricted in areas occupied by macrophages that are the known contributors to the development of pulmonary fibrosis.
The scientists depleted the Mbd2 gene in macrophages of mice to investigate this further, which protected the animals against pulmonary fibrosis, characterized by markedly reduced macrophage accumulation in the lung following administration of bleomycin.
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Direct administration of liposomes which are established carriers of inhaled drugs loaded with MBD2 silencer RNA into the trachea of mice protected them from lung injuries and fibrosis.
“Since MBD2 itself does not affect the essential epigenetic process of DNA methylation, inhibiting the molecule could prove to be a safe way to treat pulmonary fibrosis,” the study authors wrote.
“However, future studies will first need to assess the impact of altered MBD2 expression in other types of cells relevant to pulmonary fibrosis, they noted.