Dr Joan Taylor and colleagues from the University of North Carolina examined the role of the focal adhesion kinase (FAK) protein in the pathway through which cell damage occurs following MI.
FAK is involved in a variety of processes that help maintain cell function and integrity and is especially critical for the correct functioning of heart tissue, the researchers said.
Previous studies have found that FAK is activated in the heart after an MI and could be linked to pathways involved in inflammation and permanent damage to heart tissue.
Dr Taylor and her team used genetically modified mice to study the effect of altering FAK on damage following ischaemia-reperfusion injury.
They found that modifying FAK 'dramatically' increased activity of the protein.
This led to a reduction in the rate at which heart cells died following injury and cut the resultant infarct size in the 24 to 72 hours after the ischaemia-reperfusion injury.
The researchers hope the findings will support development of drugs and gene therapies to protect heart tissue.
'Several recently developed chemotherapeutic agents target receptor tyrosine kinases upstream of FAK,' they said. 'It will be of future importance to evaluate whether enhancing FAK activation might also be an effective strategy to preserve myocardial function.'
A variety of other approaches, including tissue conditioning and heat treatment, could also be used to enhance FAK activity, they suggested.