Doctors Proved the Human Heart Can Heal Itself After a Heart Attack

Keypoints:

• University of Sydney researchers showed human heart muscle can regrow after a heart attack
• The finding overturns the long-held assumption that damaged heart tissue can't regenerate
• Researchers used living tissue from patients undergoing heart bypass surgery
• The regeneration process, cardiomyocyte mitosis, had only been seen in mice before
• Findings were published in Circulation Research

For decades, doctors treated heart attacks with a grim assumption built in: once heart muscle dies, it's gone for good. Researchers at the University of Sydney, the Baird Institute, and Royal Prince Alfred Hospital just overturned that assumption directly, using living human heart tissue rather than animal models or postmortem samples.

The team confirmed that human heart cells can divide and multiply, a process called mitosis, after a heart attack. That kind of regeneration had been observed in mice before. Nobody had confirmed it happening in humans until now.

What made the confirmation possible was the tissue itself. Researchers collected living heart samples from patients undergoing bypass surgery, a technique that let them study real, functioning human heart cells rather than working from indirect evidence after the fact. 

First author Dr. Robert Hume, from the University of Sydney's Faculty of Medicine and Health, said the discovery reframes what scientists thought was permanently off-limits. "Our research shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities," he said.

Hume was careful not to overstate where the science currently stands. "This new discovery of regrowing muscle cells is exciting, it isn't enough to prevent the devastating effects of a heart attack," he said. 

The researchers also identified several proteins involved in the regeneration process, proteins previously linked to heart repair in mice, giving the team specific targets to study as they work toward therapies that could amplify the heart's natural repair response rather than leaving it to chance.