"Fibrosis can seriously affect the functioning of heart, lung, liver and other tissues," he added. The protein may also be important in treating other diseases resulting in severe fibrosis, including liver cirrhosis and interstitial lung disease, he said.

Greenspan, an expert on collagen, joined Thomas Sato of Weill Cornell Medical College to study mice that don't produce sFRP2 to understand how the protein works, according to Wisconsin release. When the scientists restricted blood flow to the animals' hearts, mimicking a heart attack, they found that scarring was significantly reduced in these sFRP2-free animals.

"Importantly, we found that when we reduced the level of fibrosis, heart function significantly improved in the mice," said Greenspan, also a professor of pharmacology at UW-Madison.

Identifying agents that specifically target sFRP2 and halt its activity will be a promising approach to controlling heart attack-induced scarring and impaired heart function, said Greenspan, and his lab has begun the search. The UW scientists also hope to study how sFRP2 and other proteins that enhance collagen formation may interact.