In mice that had miR-208 present at normal levels, heart damage occurred. But in the animals lacking miR-208, the heart remained healthier, at least in the short term, and levels of beta-myosin remained low.
The researchers also engineered mice to express three times the normal level of miR-208, and found that they had elevated levels of beta-myosin. Work is currently under way to see if those mice show heart damage.
MiR-208 is identical in humans, mice and other animals, indicating that it has a basic and widespread function in controlling heart damage, Dr. Olson said.
The work suggests that if miR-208 can be tied up or eliminated by therapeutic treatment, it might be a way to treat heart disease, Dr. van Rooij said. "That would be golden, because even a tiny increase in beta-myosin heavy chain in humans has been proven to diminish heart function," she said.
Although miR-208 appears to damage the heart during stress, it may have beneficial functions for maintaining normal action of heart muscle cells, Dr. Olson said. So any therapeutic approach would probably need to target its harmful stress responses while leaving normal function alone, he said.