After a heart attack, the heart tissue that is deprived of oxygen and dies does not regenerate in adult humans. This leads to a significant increase in the risk of death over the following years, with 65% of heart attack patients over 65 years old dying within eight years of the initial incident. However, researchers have identified a mechanism that allows them to treat heart tissue and make healthy mice’s hearts more resilient before a heart attack.
Most heart attacks are caused by coronary artery disease, which narrows the coronary arteries due to a gradual buildup of fatty deposits called atheroma. When a piece of atheroma breaks off, a blood clot forms around it, blocking the coronary arteries and causing heart muscle death. Scar tissue forms in place of healthy cardiac muscle, and cardiomyocytes, the cells responsible for the contraction of the heart muscle, lose some of their ability to squeeze blood around the body effectively.
Lack of Sleep Increases Heart Attack Risk
While cardiomyocytes can proliferate in human fetuses, this ability is lost in mature adult humans. Previous research into dedifferentiated cardiomyocytes, cells that are able to proliferate, has shown that they could become proliferative in a way that is similar to cancer. Researchers have hoped that redifferentiation of cardiomyocytes back to their original contractile state could avoid some of these complications, but it was unclear if the potential beneficial effects of previous differentiation to a more proliferative state would remain.
Researchers in Dr. Eldad Tzahor’s lab at the Weizmann Institute of Science Molecular Cell Biology Department have identified that when a particular protein ERBB2, coded for by the ERBB2 gene, is over-expressed, cardiomyocytes can dedifferentiate and become more proliferative. When overexpression is stopped, the cardiomyocytes undergo redifferentiation and regain their original contractile ability, improving cardiac performance. In a recent study, the researchers showed that when a transgenic mouse had its ERBB2 gene temporarily activated at 3 months old and then had a heart attack 5 months later, it recovered. This demonstrated that redifferentiated cardiomyocytes maintained some of their proliferative, and therefore healing capacity, and had a cardioprotective effect that could be significant in the future.
