Australian researchers have found the first direct evidence that human heart muscle cells can regrow after a heart attack, challenging decades of medical orthodoxy that held the organ was incapable of repairing itself once tissue was destroyed.
The study, led by cardiologist Robert Hume and senior author Professor Sean Lal at the University of Sydney, was published this week in the American Heart Association journal Circulation Research. Working with the Baird Institute and Royal Prince Alfred Hospital, the team examined living heart tissue taken from patients during bypass surgery, comparing scarred, oxygen-starved regions with healthy muscle from the same hearts.
Using gene-expression sequencing and protein analysis, the researchers found signs that cardiomyocytes — the specialized cells that contract to pump blood — were re-entering the cell cycle and dividing in the damaged tissue, something previously demonstrated only in mice. A heart attack can destroy roughly a third of the heart's muscle cells, and in Australia alone close to 144,000 people are living with heart failure while only about 115 heart transplants are performed each year, underscoring the size of the problem any regenerative therapy would need to address.
A repair system too weak to matter yet
The pre-mortem tissue-sampling technique that made the discovery possible was developed by cardiothoracic surgeon Paul Bannon and Lal, allowing scientists to study living human heart cells rather than relying on post-mortem samples or animal models. Researchers stress that the natural regenerative response is far too limited on its own to reverse the damage of a heart attack.
Our research shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities.
Robert Hume, University of Sydney
Lal's team now wants to identify the molecular signals that trigger this limited division, with the goal of developing drugs or gene therapies that could amplify it many times over. Heart failure remains one of the costliest and deadliest chronic conditions worldwide, and cardiovascular disease accounts for close to a quarter of all deaths in Australia, so even a modest boost to the heart's own repair capacity could meaningfully change outcomes for patients whose only current options are managing symptoms or waiting for a transplant.
Outside researchers have cautioned that the finding, while significant, is an early mechanistic result rather than a treatment. Confirming the effect in larger patient cohorts, and translating it into a therapy that safely and selectively drives cardiomyocyte division without triggering uncontrolled growth, could take years of further work. The Sydney team says its next studies will focus on the specific molecular pathways behind the division signal, with an eye toward eventually testing whether it can be pharmacologically boosted in patients recovering from a heart attack.
