Promising Reversal of Lung Fibrosis in Mice

Fibrosis Reversed in Mice Using Existing FDA-Approved Drug

Lung fibrosis is a lung condition involving too much scarring that affects people’s breathing and currently can not be treated. But now, scientists at the College of Alabama have discovered a way to turn around the problem in mice, utilizing a drug currently available for various other usages.

In patients with idiopathic lung fibrosis (IPF), lung tissue comes to be marked due to an uncommon recovery process that transfers way too much collagen. That lowers lung cells’ capacity to absorb oxygen from the air, resulting in shortness of breath, coughing, fatigue, and breast discomfort. Treatment can reduce the development of the disease, yet there’s no cure, as well as it has a high death rate within a couple of years.

Reversing Lung Fibrosis: Promising Results with ABT-199

However, in the new study, researchers have found a method to reverse the condition in mice completely. The trick is a medicine called ABT-199, which, comfortably enough, has already been accepted by the FDA for use in treating some sorts of leukemia. The team treated mice with lung fibrosis with a daily dose of ABT-199, and also after 21 days, their architecture had gone back to typical, without any collagen deposition.

The researchers discovered after seeing that human people with IPF had higher amounts of a healthy protein called Bcl-2 in their lung immune cells. Bcl-2 manages apoptosis, the procedure of set cell death, and raised degrees of this protein meant that the immune cells, called macrophages, refused to die off when their work was done. This seemed to lead to the damage of IPF.

To evaluate the correlation, the group then crafted computer mice to do not have the Bcl-2 gene. Sure enough, these computer mice seemed to be protected from pulmonary fibrosis caused by asbestos and certain medicines that generally trigger the problem. This ultimately led the scientists to evaluate ABT-199, which functions by preventing Bcl-2.

While the work is still in the extreme onset, the team claims it might open a new target for future treatments for lung fibrosis in human beings.

The research was published in the Nature journal Cell Death & Differentiation.

Source: University of Alabama