Blocking BCAT1 enzyme reduces heart scar tissue in mice
Investigators in Japan identified the enzyme BCAT1 as a key driver of cardiac fibrosis after heart injury. BCAT1 helps myofibroblasts supply proline for collagen production, and blocking it in mice reduced scar formation and helped preserve heart pumping function. The results, published in the Journal of Clinical Investigation, suggest BCAT1 as a possible target for treating fibrosis.
After cardiac injury, repair relies on collagen-rich scar tissue, but too much collagen makes the heart stiff and weakens pumping. Fibrosis also occurs in organs such as the liver and can progress to cirrhosis; it is linked to a large share of deaths in developed nations, yet no established treatment directly addresses it.
In mice, BCAT1 was scarce in healthy hearts but rose in collagen-producing myofibroblasts after a heart attack. Because proline makes up about one-fifth of collagen, BCAT1 helps sustain that building block. Removing BCAT1 or giving ERG240 lessened scarring and protected heart function, even when started a week after injury.
If BCAT1 inhibition translates to humans, patients with heart attack-related damage or fibrotic conditions such as liver cirrhosis might benefit from treatments that limit scarring while preserving organ function. Clinicians and drug developers may gain a new target, though mouse results require human trials. Because fibrosis contributes to many deaths, even partial control could ease long-term disability and healthcare burdens, but safety and timing remain uncertain.