Japanese Researchers Identify Enzyme Target That Could Limit Heart Damage After a Heart Attack
Japanese researchers at Nagoya University have identified an enzyme that could become a target for treatments designed to reduce harmful scarring of the heart after a heart attack, potentially helping preserve its ability to pump blood.
The enzyme, known as BCAT1, appears to contribute to cardiac fibrosis, a process in which excess scar tissue develops in the heart. Although scar tissue is essential for repairing damaged heart muscle, excessive buildup can stiffen the heart and impair its function, increasing the risk of heart failure.
The researchers found that BCAT1 helps supply proline, an amino acid required for collagen production. Collagen is a major component of the scar tissue that forms during the heart’s healing process.
In experiments involving laboratory mice, inhibiting BCAT1 reduced scar tissue formation after a heart attack. The treated animals also retained better heart function than those in which the enzyme remained active.
The research team used a compound called ERG240 to inhibit the enzyme. Notably, the treatment showed effects even when it began seven days after the heart attack, when the scarring process was already underway.
The researchers also examined heart tissue samples from patients with heart failure and found increased levels of BCAT1 in areas showing significant fibrosis. This finding provides additional evidence of a potential link between the enzyme and harmful scar tissue formation, although it does not establish that BCAT1 inhibition will improve outcomes in patients.
The findings could help guide the development of future treatments aimed at reducing the risk of heart failure following a heart attack.
However, the research remains at an early stage. The reported benefits are primarily based on animal experiments and analyses of human tissue samples. Further studies are needed to establish whether targeting BCAT1 is safe and effective in people.
If future clinical trials confirm the results, targeting this enzyme could offer a new approach to protecting heart function after a heart attack.
