What did this heart study do differently from previous research?

Previous cardiac studies used post-mortem tissue, losing active molecular signals. This team collected tissue from living bypass surgery patients and preserved it in liquid nitrogen within fifteen minutes, capturing cell division activity that post-mortem sampling misses.

How long until a heart regeneration treatment is available?

There is no clinical treatment yet. The team identified proteins linked to cardiomyocyte division as drug targets, and the living tissue model is now a tool for testing compounds. Clinical translation from this type of foundational finding typically takes years of further research.

Heart muscle grows back after a heart attack — confirmed in humans for the first time

Q: Why can't doctors already fix heart failure?

Heart failure results from irreversible muscle loss. The heart compensates by working harder, which eventually fails. A heart transplant is the only cure, and donor organ supply is severely limited — roughly 144,000 Australians live with heart failure against approximately 115 transplants performed each year.

A heart attack destroys, on average, roughly one third of the muscle cells in the affected chambers. That loss has always been considered permanent. Cardiac muscle, unlike the liver or skin, was thought to have essentially no capacity to replace what a major injury takes. The scarring that forms over damaged heart tissue was the story’s final chapter.

It turns out there is another chapter. Researchers at the University of Sydney, working with living heart tissue taken from patients during bypass surgery, have confirmed what had only ever been seen in mice: after a heart attack, the human heart begins producing new muscle cells.

The finding does not mean the heart heals itself. The regenerative response is far too small to offset the scale of the damage. But proving the capacity exists changes what researchers can target — and raises the possibility that a therapy could one day amplify what the heart already tries to do.

How they measured it

The difficulty with studying human heart tissue has always been a timing problem. By the time a post-mortem sample reaches a laboratory, the molecular signals of active cell division have largely dissipated. Dr. Robert Hume, the study’s first author and a researcher at the Baird Institute for Applied Heart and Lung Research, helped solve this by developing a sampling approach that collects tissue from living patients.

Consenting patients undergoing bypass surgery at Royal Prince Alfred Hospital in Sydney agreed to have small tissue samples taken from both damaged and undamaged areas of their hearts during the procedure. The samples were preserved within fifteen minutes using liquid nitrogen, which locked the biological activity in place. That level of fidelity, impossible with post-mortem material, allowed the team to detect what earlier studies had missed: a statistically significant increase in cardiomyocyte mitosis — the process by which muscle cells divide and reproduce — in the hearts of patients who had experienced infarctions.

“We were able to show a statistically significant increase in cardiomyocyte mitosis in infarcted human hearts,” Dr. Hume noted. Scientists had previously observed the same effect in mice. This is the first time it has been documented directly in human tissue.

What heart attacks actually destroy

The scale of the problem explains why this finding matters even if the regenerative signal is modest. A severe heart attack can eliminate as many as one billion cardiomyocytes — cells that the heart relies on to beat and to coordinate timing across chambers. The muscle that survives has to compensate, often by stretching. Over years, that compensation fails. The heart enlarges, weakens, and its ability to pump blood to the rest of the body declines.

That endpoint is heart failure, and it has no straightforward fix. Australia alone has approximately 144,000 people living with the condition. Transplantation is currently the only definitive treatment, and the country performs roughly 115 such procedures each year. The gap between need and supply cannot close through surgery alone.

Cardiovascular disease remains the leading cause of death worldwide. Any therapy that changes the odds after a heart attack — even modestly — would reach a population in the tens of millions.

Why this doesn’t settle the question

The heart’s natural regenerative response, as currently understood, cannot keep pace with the injury that triggers it. The cell death caused by a major infarction far exceeds the number of new cardiomyocytes the heart generates in response. Dr. Hume acknowledged this directly: the regenerative response, while real, is not sufficient to prevent the heart from being left scarred.

There is also a question of mechanism that the field has not fully resolved. Related research in failing human hearts has found that many of the DNA replication events in cardiomyocytes involve polyploidization — cells accumulating extra copies of their genome without actually splitting — and multinucleation, rather than standard mitotic division. Separating genuine proliferation from these related but distinct processes is part of the technical challenge the Sydney team’s living tissue model is now positioned to address.

The research also drew on a specific patient population — people already undergoing bypass surgery — who may not represent the full spectrum of heart attack patients. Larger, more diverse studies will be needed to understand how consistently this regenerative signal appears and whether it differs in younger patients, those with different infarct sizes, or those treated early versus late.

What the proteins suggest next

The team also identified several proteins in the human tissue that had previously been linked to cardiac regeneration in mice. Those proteins offer the most concrete early lead for therapy development. If they are the molecular switches that trigger cardiomyocyte division in response to injury, they become targets — things a drug might activate or amplify.

Professor Sean Lal, senior author of the study and a heart failure cardiologist at Royal Prince Alfred Hospital, described what the team is working toward: “Ultimately, the goal is to use this discovery to make new heart cells that can reverse heart failure. Using living human heart tissue models in our work means that we will have more accurate and reliable data to develop new therapies for heart disease.”

The living tissue model is itself now a research tool independent of this single result. Because it preserves the molecular state of the heart at the moment of surgery, it can be used to test compounds that might boost cell division — without requiring another human to have a heart attack first.

Common questions about heart regeneration

Can the human heart repair itself after a heart attack?

The heart has a limited, natural capacity to grow new muscle cells post-infarction, as this study confirms for the first time in human tissue. The regeneration occurs through cardiomyocyte mitosis — cell division. The number of new cells produced is far too small to replace the muscle lost during a major infarction, so the heart’s repair response exists but is functionally insufficient on its own.

Why can’t doctors already fix heart failure?

Heart failure results from irreversible muscle loss: the heart compensates for weakened areas by working harder, which eventually fails. A heart transplant is the only cure, and donor organ supply is severely limited. Roughly 144,000 Australians live with heart failure against approximately 115 transplants performed each year. The gap between patients and available organs drives the search for therapies that could regenerate damaged muscle.

What did this study do differently from previous research?

Previous studies of cardiac regeneration used post-mortem tissue. By the time those samples reach a laboratory, the molecular signals of cell division have faded. The Sydney team collected tissue from living patients during bypass surgery and preserved it within fifteen minutes using liquid nitrogen. That approach captured active biological processes that post-mortem sampling misses — including the cell division signal that is the study’s central finding.

How long until a treatment is available?

There is no clinical treatment based on this finding yet. The team has identified proteins that may regulate cardiomyocyte division, and these are now targets for drug development. The significance of this work is that it opens a therapeutic direction previously considered closed: the adult human heart can make new muscle, and researchers now have a tool to study how to make it do so at useful scale.

The next phase of the research will attempt to identify which proteins can be amplified in the living tissue model, and whether doing so increases the rate of cell division to levels that could realistically offset infarct damage.

Tags: biology, cardiac regeneration, cardiology, cardiomyocyte, heart attack, heart failure