Discovery of an enzyme that limits cardiac fibrosis after heart attacks
Amman2 min read
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Scientists from Japan's Nagoya University have found that inhibiting the BCAT1 enzyme may reduce the formation of scar tissue in the heart following a heart attack, helping to maintain its ability to pump blood.
After a heart attack, parts of the damaged heart muscle are gradually replaced by connective tissue rich in collagen, a natural process that helps heal the tissue. However, excessive formation of this tissue leads to cardiac fibrosis and increased stiffness of the heart muscle, which impairs its functional efficiency.
Experiments conducted on mice showed that the BCAT1 enzyme contributes to the development of fibrosis by providing proline, an amino acid essential for collagen production. The results also demonstrated that disabling this enzyme reduces scar formation and preserves heart function better compared to normal mice.
The researchers used the inhibitor ERG240 to disable the enzyme's activity and observed that it remained effective even when treatment was started seven days after the heart attack, i.e., after the scar tissue had begun to form.
Furthermore, an analysis of heart tissues from patients suffering from heart failure revealed elevated levels of BCAT1 in areas where fibrosis is clearly present.
The researchers believe that targeting this enzyme may pave the way for developing new therapeutic approaches to limit cardiac fibrosis and prevent heart failure after heart attacks; however, these results still require further studies to confirm their efficacy and safety in humans.
