A team of Israeli researchers has developed a procedure that prevents heart attacks. The only problem? It’s just that, for now, they’ve only managed to do it in mice.
Scientists have activated a cellular mechanism in the hearts of healthy mice that makes them resistant to future heart attacks – even when they occur months later, explains the The Jerusalem Post. The procedure performed on healthy rats improved their recovery from subsequent cardiac injuries.
Still, although the leap from mouse to human is great, is an important first step in this direction. Rats are often used as guinea pigs in early laboratory tests.
The authors of the study, however, warn that until the procedure is applicable in human beings there are still a few years to go. Still, the study results profoundly change our understanding of the regenerative capabilities of the heart and possibly other organs.
“It’s a proof of concept”, says author Eldad Tzahor. “It points to new avenues of investigation that look at treating the heart not just after damage has occurred, but from a preventative perspective that increases the ability to recover from an injury before it even occurs.”
The study focuses on genetically modified mice, whose cardiomyocytes they overexpress a gene that triggers cell division—a phenomenon that also affects humans.
Earlier, scientists in Tzahor’s laboratory had discovered that the gene ERBB2 causes cell division in cardiomyocytes. Something remarkable, given that shortly after birth, these cells lose the ability to multiply.
Heart attacks kill large numbers of cardiomyocytes that the body cannot regenerate. After in previous studies, Tzahor’s team was not able to recover the heart function of mice, this time tried a different approach.
In this study, published in the journal Nature Cardiovascular Research, the scientists sought to understand what happens to hearts “rejuvenated” by ERBB2 and how, exactly, they return to normal function after the gene is turned off.
“It was surprising and curious. We had assumed that everything would go back to normal after ERBB2 was turned off in cardiomyocytes. Yet here we were, seeing a different genetic pattern – overexpression in some genes and underexpression in others – following ERBB2 activation. In other words, we found long-term effects.”
Instead of turning on ERBB2 in diseased mice to make their cardiomyocytes divide, the authors first turned it on in healthy mice for a few weeks and then turned it off again.
The result was that mice that were engineered to overexpress ERBB2 recovered, but others did not. “The results left us speechless”, Tzahor told the Israeli newspaper. “We found a cardiac fountain of youth in those mice, a new way to make the heart younger and stronger.”
ZAP // 
