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Normal scar tissue forms to heal an internal wound and quietly retreats after healing. But in many common diseases like kidney, liver and lung fibrosis the scar tissue goes rogue and strangles vital organs. These diseases are largely untreatable and ultimately fatal.
Fibrosis is a progressive scarring and hardening of internal organs, it may cause 40 percent of deaths across the globe. Fibrotic diseases include diabetic kidney fibrosis, alcoholic liver cirrhosis, hepatitis C, pulmonary fibrosis and nonalcoholic fatty liver disease, which may lead to fibrosis of the liver-the leading cause of liver transplant.
In one subset of human fibrosis cells, scientists discovered a delinquent molecules that continually shouted at an immune receptor, the antennae on the cell to produce scar tissue instead of quieting down and allowing the scar tissue to go back to sleep. Scientists collaborated with a University of Colorado researcher who used crystallography and computer modeling to predict a molecule that could block the receptor that leads to the uncontrolled scarring.
When they tested the molecule, T53, in three different mouse models of fibrosis, the abnormality was significantly reversed. The leading cause of liver failure is liver fibrosis. Most fibrotic disease likely begins as normal repair of an injury, but if the immune system produces too much of an initial scar, it can’t go back to normal, an unhealed scar that keeps growing can wipe out the entire organ.
Not all fibrosis is caused by the same abnormality, if the compound-T53, is eventually developed into an approved drug, it would be targeted to patients with the specific genetic signature identified in the study. There is an emerging direction for treating fibrosis with precision medicine. Some people live with fibrotic disease for 30 years while others die in two years.