Seven to eight percent of heart muscle cells divide after a heart attack. An Australian research team has shown this for the first time using tissue samples from living patients, as ScienceDaily reported on September 9, 2026. For decades it was considered impossible that cardiomyocytes divide. For clinically relevant regeneration, 25 to 50 percent would be needed. The finding shows: the heart begins repair but falls short on intensity. That is precisely where research can intervene.
What happens in the heart after a heart attack
Up to four million people in Germany suffer from heart failure according to the German Heart Report 2025, and nearly 44,000 people die from acute heart attack here each year. The mechanism is always the same: when a heart blood vessel clogs and oxygen is cut off, heart muscle cells, known as cardiomyocytes, die within minutes. Scar tissue forms in their place, unable to contract, and the heart pumps permanently weaker.
For decades, medical teaching held: these cells are lost forever. This assumption rested almost entirely on autopsy data, tissue samples taken hours after death. The problem: signal molecules indicating cell division break down quickly in dead tissue. Whether the heart of living patients actually attempts to replace cardiomyocytes could not be reliably measured this way.
Live tissue instead of autopsy: the crucial method
That is precisely where Professor Paul Bannon and Professor Sean Lal from the University of Sydney and the Baird Institute intervened. They developed a method in which tissue samples from infarcted and healthy heart tissue were taken during bypass operations or shortly after stopping life-support measures. These pre-mortem biopsies preserved the molecular signals intact, signals that fade away in autopsy samples.
The University of Sydney published the results in Circulation Research, volume 138, under the title "Human Hearts Intrinsically Increase Cardiomyocyte Mitosis After Myocardial Infarction". And the finding delivered what this title promised: in samples from infarcted heart sections, 7 to 8 percent of cardiomyocytes showed mitosis, that is, active cell division. Among them were cells in all phases of the division process, including cytokinesis, the step where the cytoplasm divides into two daughter cells.
The gap between 7 and 25 percent
This finding is clear but also sobering when considering magnitude: expert literature suggests that 25 to 50 percent of cardiomyocytes must be newly formed after an infarction for the heart to functionally regenerate. Seven to eight percent is real, but nowhere near sufficient.
At the same time, samples from non-infarcted areas were substantially lower, showing: the heart responds specifically to injury. There is a biological switch that activates cell division after an infarction. This switch works, it is simply not strong enough. And that is where research can intervene.
In comparison: zebrafish, newborns, and the adult human
The ability to regenerate heart tissue is evolutionarily ancient. Zebrafish can regenerate up to 20 percent of their heart ventricle and recover nearly completely within 30 to 60 days. Instead of scar tissue, functional muscle tissue forms. Salamanders show similar abilities.
Even more instructive is a comparison within mammals: newborn mice can fully regenerate their hearts immediately after birth. By the seventh day of life, this ability is already gone: cardiomyocytes stop dividing and remain permanently at rest. The same applies to other mammals, presumably including humans. What the Sydney study now shows: the mechanism is not completely shut down in the adult heart. It runs after an infarction at around 7 to 8 percent capacity, a faint echo of neonatal ability, but not a dead switch.
From 7 to 8 to 25 to 50 percent: the next step in research
The research goal is clearly stated: identify the molecular signals that trigger the 7 to 8 percent mitosis after infarction and find ways to raise this to 25 to 50 percent. Professor Sean Lal explained in a Sydney Morning Herald report that the research goal is to use this discovery to generate new heart muscle cells that could reverse heart failure. Growth factors like IGF2, which also play roles in neonatal regeneration, are considered known candidates for the underlying signaling pathways.
Between proof of principle and approved therapy typically lies ten to fifteen years. What the Sydney study changes is the starting point: whoever seeks a way to strengthen something must first show it exists. That has now, for the first time with tissue from living humans, been accomplished.