Further, Jun was able to "rescue" the mutated mice by applying CCN1 protein topically to the skin wound, triggering fibroblast senescence and limiting the formation of scar tissue.

The discovery that senescence is a normal wound-healing response in the skin; that senescence in the wound serves an anti-fibrotic function; and that CCN1 is the critical protein that controls this process may prove important in understanding a wide range of pathological conditions related to tissue scarring, said Lau.

"For example, chronic injury to the liver from a number of causes, including viral infections, alcoholism, diabetes and obesity, leads to fibrosis and may progress to cirrhosis," Lau said. "After a heart attack, accumulation of scar tissue in the heart impairs its ability to pump efficiently."

The ability to control the formation of scar tissue, or fibrosis, has important implications for future therapies for treating wound-healing disorders, including organ damage where functional tissue is replaced with scar tissue, Lau said.

Source: University of Illinois at Chicago