Protein That Delays Fatal Lung Disease, Identified
A protein has been discovered that can delay the progress of pulmonary fibrosis and promote longer patient survival, according to a recent scientific study.
The study, published in the American Journal of Respiratory and Critical Care Medicine, details how patients suffering from pulmonary fibrosis with naturally high levels of the protein LYCAT in their blood have significantly better survival rates and lung function, compared to patients with lower levels of the protein.
Pulmonary fibrosis is a fatal lung disease that progresses as the lungs become covered in scar tissue. There are a number of different causes for this including persistent infection, undesirable autoimmune responses (inflammation), and damage from certain gases. According to the US Centers for Disease Control and Prevention, due to industrial workers breathing in fine metal dust, the disease was commonly seen among workers in metal coating-plants around the late 1900s, before stricter safety regulations limited the chances of the occupational hazard.
According to researchers from the University of Illinois at Chicago (UIC), the disease still affects people today, but treatment options and preventative options are limited, and the cause of the disease can vary.
Previous research identified several genes that may be involved in the development of a variation of pulmonary fibrosis -- referred to as IPF -- that has no apparent cause. In the latest study, UIC researchers investigated a protein LYCAT (lysocardiolipin acyltransferase), which is produced by one of the previously identified genes.
To assess the effects LYCAT has on pulmonary fibrosis patients, the researchers measured the protein's prevalence in the blood of several IPF patients. Interestingly, the researchers found that IPF patients with higher LYCAT levels survived longer with slower disease progression, compared to patients with lower levels of the protein.
Long Shuang Huang, the first author of the paper, explained in a UIC news release that this shows that the protein may be working as a protective measure against progression of the disease, and the genetic mutations associated with IPF may actually be limiting the production of this protein.
"This suggests that boosting LYCAT levels in patients with pulmonary fibrosis may be a viable new therapeutic approach to treating the disease," Huang said.
The study was published in the American Journal of Respiratory and Critical Care Medicine on April 29.
The UIC news release was published on May 6.