According to estimates, fibrotic diseases including diabetic kidney fibrosis, alcoholic liver cirrhosis, hepatitis C, pulmonary fibrosis and nonalcoholic fatty liver disease, contribute to almost 45 to 50 per cent of deaths globally.
The team from Northwestern University in the US, discovered a delinquent group of molecules that continuously affected an immune receptor -- the antennae on cell -- to produce scar tissue instead of allowing it go back to sleep.
They then identified molecule T53, which, when tested in three different mouse models of fibrosis, reversed the abnormality significantly.
"Our study opens a new door into fibrosis by looking at it as an aberrant innate immune response and suggesting a novel approach to treat it," said senior author John Varga from the varsity.
Most of the times, fibrotic disease likely begins as normal repair of an injury, scientists said.
"But if the immune system produces too much of an initial scar, it can't go back to normal. You have an unhealed scar that keeps growing and can wipe out the entire organ," Varga explained.
"We are not saying this compound is ready to be a drug. It's an initial compound that would need to be developed and tweaked," Varga added, in the paper published in Journal of Clinical Investigation Insight.
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