
AI-generated summary
After a heart attack, damaged areas of the heart muscle are replaced with connective tissue containing collagen, which is necessary for healing, but excess leads to fibrosis and impaired cardiac function.
Blocking the BCAT1 enzyme helped reduce the formation of scar tissue in the heart after a heart attack and preserve its ability to pump blood. This conclusion was reached by scientists from Nagoya University in Japan during experiments on mice. The study results were published in the Journal of Clinical Investigation (JCI).
After a heart attack, damaged areas of the heart muscle are gradually replaced by connective tissue containing collagen. This process is necessary for healing, but excessive scarring causes the heart muscle to harden and not function properly. The researchers found that the enzyme BCAT1 promotes such fibrosis by providing cells with proline, an amino acid necessary for collagen production.
In experiments, mice with the BCAT1 gene disabled after a heart attack formed less scar tissue and better preserved cardiac function compared to normal animals. A similar effect was observed when using the ERG240 inhibitor, which blocks the enzyme. Moreover, the drug turned out to be effective even in cases where treatment began seven days after a heart attack, that is, after the formation of scars began.
Analysis of heart tissue from patients with heart failure also revealed increased levels of BCAT1 in areas of severe fibrosis. According to scientists, suppressing the activity of this enzyme may become the basis for a new method of preventing heart failure after a heart attack.
AI outlook — possibilities, not facts
Clinical trials of the ERG240 inhibitor will begin in the next two years
Possible · Within years

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