Focal adhesion kinase, or FAK protein could reduce the damage caused by heart attack by about 50 per cent.
Researchers from the University of North Carolina at Chapel Hill conducted a mouse study on the protective protein, which is found in both mice and humans.
"This study shows that we can enhance existing cell survival pathways to protect heart cells during a heart attack," said Joan Taylor, PhD, associate professor in UNC's department of pathology and laboratory medicine.
She added that the findings could lead to new treatment approaches for heart attacks and may have broad implications for scientists seeking to manipulate the body's natural defensive systems.
During a heart attack, oxygen-deprived heart cells emit signals that activate the usually inert protein FAK. If it arrives on time, it can save the cell and reduce permanent damage to the heart.
"We thought if we could activate FAK to a greater extent, then we could better protect those heart cells," said Taylor.
Based on their previous studies that defined the signals induced by FAK in heart cells, they reasoned that expression of FAK set to an "always-on" position would eventually suffer uncontrolled inflammation and heart failure.
The researchers then adjusted their formula to create a new protein they called "SuperFAK". To enhance its protective abilities without the harmful side effects, SuperFAK was primed for activation - ready to rush to the scene at the slightest provocation from stressed heart cells - but remained under the control of the mice's natural feedback systems that would shut it off when the crisis passed.
Mice with SuperFAK showed a much stronger FAK response during a heart attack than mice with the natural protein, and three days later had about 50 percent less heart damage. Critically, SuperFAK deactivated at the appropriate time, so the eight-week follow-up revealed no detrimental effects.
The findings offer evidence that, rather than simply activating or de-activating key proteins, researchers can benefit from a more nuanced approach that taps into the body's natural feedback loops.
"I think folks could use this idea to exploit mutations in other molecules -by thinking about how to modify the protein so that it can be under natural controls.
"Negative feedback loops are important because they 'reset' the system," said Taylor.
The findings also may help researchers augment FAK in patients undergoing chemotherapy. Some chemotherapy drugs are known to break down FAK, leaving patients' hearts more vulnerable to damage.
The study appeared on March 1 in the online edition of the journal Arteriosclerosis, Thrombosis and Vascular Biology.