Lung scarring, also known as lung fibrosis, is a serious condition where parts of the lungs become thickened and stiff.
This happens because scar tissue forms in the lungs, which makes it hard to breathe.
The most common type of lung scarring is called idiopathic pulmonary fibrosis (IPF), which means its cause is unknown.
People with IPF often experience increasing difficulty in breathing, a persistent dry cough, and extreme tiredness.
Sadly, once diagnosed, people usually live only between three to five years as there is no cure for the disease yet.
Given the severity of the condition, doctors and researchers are actively looking for ways to prevent the disease or at least slow its progression.
A team from the University of Michigan Medical School, led by Dr. Sean Fortier and Dr. Marc Peters-Golden, recently made some promising discoveries in this area.
Their study focused on a natural process that the body uses to heal wounds. Interestingly, they found that this process might be able to reverse lung fibrosis. They conducted experiments on mice, using a drug called bleomycin which is known to cause lung damage similar to IPF.
Over about six weeks, the mice’s lungs began to heal from the scarring. Dr. Fortier pointed out that understanding how fibrosis heals naturally in mice can help identify new treatment targets for IPF.
One key player in whether lung injury leads to healing or results in scarring is a type of cell called a fibroblast. These cells are usually involved in making connective tissues. When there’s damage, fibroblasts turn into a more active form called myofibroblasts, which create scar tissue.
Normally, after their job is done, these cells turn back to their inactive state or get removed from the body—a process necessary to stop continuous scarring.
Dr. Fortier explained that in conditions like IPF, these myofibroblasts don’t deactivate as they should, which leads to ongoing scarring. His team studied a specific molecule called MKP1, which helps in turning these cells off. They noticed that in fibroblasts from IPF patients, MKP1 levels were unusually low.
To further explore this, the researchers used genetic techniques to reduce MKP1 in mice after they had lung injury. They observed that without MKP1, scarring continued unchecked, confirming its crucial role in naturally ending fibrosis.
In addition, they used a gene-editing technology called CRISPR to understand how MKP1 works. They found that it mainly controls an enzyme involved in stress response, helping to shut down the scarring process.
Interestingly, current medications approved for treating lung fibrosis, such as pirfenidone and nintedanib, don’t seem to affect myofibroblasts directly.
They can slow down the disease’s progression, but they don’t stop or reverse it. This highlights the need for new treatments that can directly turn off the pathways leading to scarring.
Dr. Fortier is hopeful that this new understanding of how fibrosis can be reversed will lead to the development of better treatments.
He notes that while preventing lung scarring is important, finding ways to reverse existing scarring is crucial, as most patients already have significant scarring by the time they are diagnosed.
This research opens up a hopeful avenue for people suffering from IPF and similar lung conditions, suggesting that one day it might be possible to not just stop the progression of lung fibrosis but to reverse it, giving patients a better quality of life and possibly longer survival.
If you care about lung health, please read studies about marijuana’s effects on lung health, and why some non-smokers get lung disease and some heavy smokers do not.
For more information about health, please see recent studies that olive oil may help you live longer, and vitamin D could help lower the risk of autoimmune diseases.
The research findings can be found in the Journal of Clinical Investigation.
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