Enzyme inhibitor limits scarring after heart attacks and protects heart function in mice
Researchers in Japan have identified the enzyme BCAT1 as a key driver of cardiac fibrosis following heart attacks. Blocking this enzyme in mice successfully reduced scar tissue formation and preserved heart function, offering a potential new therapeutic target for heart disease.
Why it matters
Fibrosis is a major contributor to mortality in developed countries, and this discovery could lead to the first definitive therapy for preventing heart failure after injury.
edited by Sadie Harley , reviewed by Robert Egan
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Add to Preferred Sources Heart tissue sections stained with Picrosirius red, which highlights collagen in red, 28 days after sham surgery (left) or a heart attack (right). Following a heart attack, mice lacking BCAT1 (bottom row) show less collagen deposition than normal mice (top row), indicating that BCAT1 contributes to cardiac fibrosis after injury. Credit: Adapted from Takizawa et al., Journal of Clinical Investigation , 2026 (Figure 8E, histology panels only). CC BY 4.0. Heart failure often develops after a heart attack because excessive collagen-based scar tissue forms during repair. While collagen is necessary to reinforce scars, disease and chronic inflammation can cause overproduction, which stiffens the heart muscle and impairs its pumping ability.
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