Researchers led by Cincinnati Children’s Hospital Medical Center have discovered the molecular process behind a dangerous loss of cardiac muscle that could aid astronauts during long space flights.
"NASA is very interested in cardiac atrophy," says Jeffery Molkentin, PhD, Co-Director of the Heart Institute at Cincinnati Children's, and author of the paper.
"It might be the single biggest issue for long-period space flights and astronaut health, especially when re-entering a higher-gravity situation, whether that's arriving at Mars or returning to Earth."
To tackle loss of muscle mass, astronauts and cosmonauts currently have rigorous exercise regimes while in space. This became protocol ever since the first space flights, after which doctors realized that returning astronauts were often barely able to walk upon returning to Earth, and had an increased risk of cardiac problems after arriving back from space.
For the study, the researchers studied mouse models to trace the molecular process behind cardiac atrophy. In doing so, they identified a three-way process that can lead to a rapid and lethal loss of heart mass in mice.
Firstly, overexpression of the gene, thrombospondin-1, activates a signalling protein known as PERK. Excessive PERK activity then triggers a response from the transcription factor ATF4.
This sequence then goes on to program heart muscles to atrophy. The longer these genes are activated, the more muscle mass atrophies. The researchers say that being able to block or reduce this response could be a new way to address the loss of heart muscle during space travel.
While interesting findings , the researchers warn that they still need to confirm whether the same process occurs in people. While it is currently not possible to replace lost heart muscle tissue, it may be possible to rehabilitate weakened or atrophied heart muscle cells to properly function.
"Our findings describe a new pathway of muscle mass loss," says Molkentin. "More research is needed to develop methods or drugs that can interrupt this signaling pathway through these genes to stop cardiac atrophy once detected."