In a recent study led by Saint Louis University, researchers from around the U.S., which included co-author Joseph H. McCarty, Ph.D., of the University of Texas M.D. Anderson Cancer Center, discovered a new potential therapeutic way to treat fibrosis by deleting a gene that is critical for the development of the disease. The study was published on November 10th in the online edition of Nature Medicine.
Fibrosis could be caused by excessive forming of fibrotic tissues in organs and prevents normal functioning by making them hard. Currently, drug treatments do not exist for fibrosis and the only effective means of treatment is a transplant.
In the study, researchers successfully deactivated a protein called Transforming Growth Factor (TGF) beta, which stimulates myofibroblasts, cells which produce excess collagen for forming scars. They could remove a gene for alpha v integrins, proteins that are essentioal for TGF functioning. In addition, the researchers found that the deletion of the gene is replicable by treating with small molecular compounds, which selectively inhibit alpha v integrins.
“We have developed small molecular compounds that selectively inhibit these integrins, which suppress TGF beta protein, and these have been effective in animal models of lung and liver fibrosis,” Griggs added, according to an article on Eurekalert. “The small molecule was not only able to prevent fibrosis; it made fibrosis less severe even when the treatment was started after fibrosis had begun.”