Cell research at Brigham & Women's points to a new drug target for fibrosis

Studying the development of organ myofibroblasts in animals, a group of investigators at Brigham & Women's Hospital says that they've identified progenitor cells that may lie at the root of fibrosis--offering a new target for drug developers for a common and very serious scarring condition.

Senior author Benjamin Humphreys says their work led them to the hedgehog signaling pathway and a gene called Gli1, which was "specifically expressed in a rare group of cells located around blood vessels in all solid organs."

Working on the hypothesis that the cells play a role in fibrosis, the team says they "tagged this protein in tissue with varying forms of fibrosis, and found that these cells proliferated by almost 20-fold under chronic injury and turned into myofibroblasts."

"We believe that this cell population is responsible for about 60 percent of all organ myofibroblasts," said Humphreys

By ablating Gliu1 in mice using a genetic strategy, Humphreys said they were able to reduce signs of fibrosis and rescue heart function.

"We've found that these Gli1 progenitor cells differentiate into myofibroblasts, and in fibrotic disease, when they are ablated, we can rescue organs and organ function," said Humphreys.

The same genetic strategy, though, won't work in humans, leaving future research to find a drug that can shut down the cells and possibly advance a new therapy for fibrosis.

- here's the release

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