Broken hearts may be able to mend themselves.
Given the right biochemical motivation, stem cells in a thin layer of cells lining the outside of the heart muscle can replace a small number of the cells damaged by a heart attack, an international group of scientists reports online June 8 in Nature. A small protein called thymosin beta-4 can provide just the sort of stimulus needed to turn dormant stem cells into Mr. Fix-its, Paul Riley, a British Heart Foundation researcher at University College London, and his colleagues found.
Scientists have been searching for ways to make the heart heal itself, but previous evidence for the presence of stem cells within heart muscles is controversial, says Deepak Srivastava, a cardiac stem cell biologist at the Gladstone Institute of Cardiovascular Disease and University of California, San Francisco, who was not involved in the study. And stem cells transplanted into hearts often don’t integrate correctly, beating out of time with native cells. That’s why the new discovery that the lining of the heart has stem cells with self-healing properties is so exciting. “The notion that the heart can regenerate itself is very powerful,” Srivastava says.
Giving thymosin beta-4 to mice after a heart attack has already been shown to have the beneficial effect of helping more heart muscle survive. The new study shows that the protein may not only protect heart cells from further injury, but may also generate a few new muscle cells from stem cells in the lining, called the epicardium.
“Even though it’s a small number, it’s still significant, because we didn’t think the heart could do this at all,” Srivastava says.
Working with mice, the researchers found that epicardial stem cells need to be primed before they make new heart muscle. Mice treated with thymosin beta-4 for a week before a heart attack produced a small number of new heart muscle cells, but mice given the drug only after a heart attack didn’t.
The finding may suggest that people who are at high risk of having a heart attack could boost their ability to recover from one by taking stem cell–stimulating drugs beforehand, Riley says. But that approach may not be very practical. For one thing, thymosin beta-4 isn’t available in tablet form; it has to be injected. Another drawback is that doctors aren’t very good at identifying people in imminent danger of a heart attack, and it’s possible that taking stem cell–stimulating drugs for long periods could have dangerous side effects.
But Srivastava bets that in the long run, the right drugs will be able to tear down barriers that keep humans from growing new hearts the way fish and frogs and other amphibians can. “We just need to unleash nature’s own potential to repair itself.”
