A new study from San Diego State University (SDSU) has revealed information on a heart protein that could play a critical role in the body’s ability to combat heart disease and recover from heart attack.

The research was published in Circulation Research and was led by Christopher Glembotski, a molecular cardiologist and the director of the SDSU Heart Institute.

In studying mice, the team found that the protein, ATF6, promotes heart cells’ ability to ward of stress-induced damage, suggesting it could be used as a treatment and prevention strategy for people at risk for developing heart disease.

Glembotski’s and other research has showed that ATF6 responds to stress created by misfolded proteins in the endoplasmic reticulum by activating catalase, an antioxidant that prevents proteins from ever misfolding. The stress is usually caused by an overabundance of reactive oxygen molecules that limit the cell’s ability to function normally, which is a primary reason for heart damage, heart disease and heart attack.

In the study, the researchers examined how heart disease developed in mice with ATF6 and those without. Results showed that heart disease caused more damage in mice lacking the protein. When the researchers artificially introduced ATF6 and catalase to mice, they showed the same protective effects as those with a working version of the gene.

Additionally, the study showed that as the mice aged, they lost levels of ATF6 and, consequently, their hearts became weaker and more prone to damage after a heart attack. Based on the findings, the researchers then created a gene therapy that boosts ATF6 production and it strengthened the hearts of the mice.

"These cellular mechanics should work very much the same way in humans," Glembotski said in a statement. "It seems to be an adaptive response of the heart that is lost with age. We think that, like the mice, human heart cells usually make some ATF6, but if they could make more—like in the young heart—the heart would be more resistant to heart disease."

In future studies, Glembotski hopes to find a method to boost ATF6 production in human hearts, saying that exercise may be the simplest way. But gene therapy is always an option too, especially in older adults.