LA JOLLA, Calif., Dec. 9 (UPI) — When liver cells are damaged, the cells are replaced by scar tissue, which is meant to wall off and repair damage in the organ. If the liver operates under prolonged stress, healthy cells are replaced by scar tissue and the liver eventually stops working.
Scientists at the Salk Institute have found a molecule that, in tests with mice, prevents a regulatory protein from spreading scar tissue that leads to liver fibrosis, and eventual cirrhosis.
Traditional therapies to treat inflammation are ineffective against the development of scar tissue in the liver because the cells can bypass the drug, according to Michael Downes, a researcher at the Salk Institute. By stopping the cause of fibrosis at the genomic level, scientists were able to stop the self-encouraging process.
“After too much damage in the liver, the scar tissue itself causes more scar tissue,” said Ronald Evans, director of the Salk Institute’s Gene Expression Laboratory in a press release. “We can actually reverse liver fibrosis in animals and are now exploring potential therapeutic applications for humans.”
The scientists found hepatic stellate cells that store vitamin A are called to the site of damaged cells by the regulatory protein BRD4.
An experimental drug called JQ1, which is currently in clinical trials for cancer treatment, blocks a group of proteins involved with cellular processes, including BRD4. Researchers tested JQ1 in mice, and it not only protected against the formation of new scar tissue, but reversed the development of fibrosis.
“Our results indicate that BRD4 is a driver of chronic fibrosis and a promising therapeutic target for treating liver disease,” Evans said. “We think this discovery may also treat fibrosis in other organs, like the lung, pancreas and kidney.”
The study is published in the Proceedings of the National Academy of Sciences.
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