"The body tries to fix the injury to the heart muscle by depositing the fibers, but this causes a greater problem," says Thomas Sato, co-senior author of the study and the Joseph C. Hinsey Professor in Cell and Developmental Biology at Weill Cornell Medical College in New York City. "This process, called fibrosis, causes the heart to become like steel, unable to contract and pump blood throughout the body.
The result can be fatal." Heart attacks cause 13 percent of deaths around the world and are the primary cause of death in industrialized countries. The researchers removed a gene called Sfrp2 from a mouse's DNA. This stopped production of the protein sFRP2. The result was that the hearts of mice without the gene produced less fibrous scar tissue following a heart attack than normal mice with the gene.
Moreover, the heart function of the gene-less mice improved more quickly. All of this encouraged the authors to conclude that the protein has a crucial effect on muscle scarring following heart attack. The Sato team worked with Daniel S. Greenspan, co-senior author and professor of pathology and laboratory medicine from the University of Wisconsin School of Medicine and Public Health in Madison, Wis.
Greenspan's component of the research discovered how the sFRP2 protein interacts with collagen, the main constituent of scar tissue. He found that the sFRP2 protein works by speeding up the processing of pro-collagen into mature collagen.
"Therapeutically, the findings mean that it is possible to create a drug that may one day inhibit the functioning of the protein in order to limit fibrosis within the heart," says Sato. "Doing so may aid in controlling the degree of scarring, and allow the heart to continue to function following [heart attack]."