A study on the let-7 gene, which plays a vital role in lung recovery and the development of pulmonary fibrosis, has been published in Nature Communications.
Pulmonary fibrosis, a condition primarily affecting adults over 50, is characterized by respiratory failure and other severe symptoms.
This disease occurs when lung damage, often caused by infections, fails to heal properly. The resulting lung stiffness impairs expansion, potentially leading to respiratory failure. Idiopathic pulmonary fibrosis, which progresses with age, is particularly concerning due to its poor prognosis and high mortality rate within years of diagnosis.
The goal of the research was to determine why AT2 stem cells, which are in charge of lung repair, malfunction. They were especially curious about how the let-7 gene, which exhibits decreased expression during the fibrosis process, relates to pulmonary fibrosis.
The group found that the let-7 gene is downregulated in mouse models of pulmonary fibrosis. Interestingly, the mice developed pulmonary fibrosis independently when this gene was removed. According to these results, the let-7 gene is essential for preserving lung health and averting fibrosis.
According to the researchers, the let-7 gene is expressed in every organ, and fibrosis frequently affects the kidneys, liver, and heart. This finding may aid in determining the reasons behind fibrosis in organs other than the lungs.
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