For many years, scientists believed that the adult human heart could not replace muscle cells lost during a heart attack. When blood flow to part of the heart is blocked, oxygen-starved cardiomyocytes, the cells responsible for contraction, die. The damaged region is then largely replaced with scar tissue, which does not contract as effectively as healthy heart muscle. This loss of pumping ability can contribute to long-term heart failure. Now, new research from the University of Sydney, the Baird Institute, and Royal Prince Alfred Hospital suggests that the human heart has a limited natural capacity to regenerate muscle cells after injury.
The key process is mitosis, the division of one cell into two new cells. Researchers found that cardiomyocytes in human hearts show increased mitotic activity after myocardial infarction, the medical term for a heart attack. In other words, surviving heart muscle cells can re-enter the cell cycle and divide following injury. Similar responses had previously been observed in mice, but this study provides evidence that the response also occurs in humans.
“Our research shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities,” said Dr. Robert Hume, first author of the study. This finding challenges the long-standing assumption that mature human cardiomyocytes are essentially incapable of reproducing after injury. Rather than being completely unable to regenerate, the adult heart appears to retain a small but measurable ability to produce new muscle cells.
This regenerative activity does not mean that the heart completely repairs itself. A major heart attack may destroy a substantial amount of heart muscle, while the natural production of replacement cardiomyocytes is currently far too small to restore all lost tissue. Scar formation still occurs, and the scarred region reduces the heart’s ability to pump blood efficiently. Therefore, the finding should not be interpreted as a cure for heart attacks or heart failure. Instead, it changes the scientific understanding of the adult heart from an organ with no meaningful regenerative potential to one with a modest but measurable repair response.
An important feature of the study was its use of living human heart tissue. The researchers obtained samples from consenting patients undergoing coronary bypass surgery at Royal Prince Alfred Hospital. They collected tissue from both diseased and non-diseased regions of the heart. This approach allowed comparisons between areas affected by cardiovascular disease and areas that were relatively healthy, while preserving biological features that may be absent in animal models or tissue collected after death.
These living tissue samples also provide a valuable laboratory model for studying the molecular signals involved in repair. The research team identified proteins associated with heart regeneration in animal studies, suggesting that related pathways may operate in people. By determining which signals encourage cardiomyocytes to divide, scientists may eventually develop treatments that strengthen the heart’s existing regenerative response. Potential future therapies could aim to stimulate production of new muscle cells, reduce scarring, or improve recovery of damaged heart tissue.
The researchers believe this discovery could eventually have implications beyond understanding how the heart responds to injury. Professor Sean Lal, senior author of the study, described the long-term goal: “Ultimately, the goal is to use this discovery to make new heart cells that can reverse heart failure.”
The clinical importance of this work is substantial because heart failure remains a major consequence of heart attacks, and treatment options for advanced heart failure are limited. Heart transplantation can be life-saving for some patients, but donor hearts are scarce. A therapy that safely increases cardiomyocyte regeneration could one day help preserve heart function after injury and potentially reduce the need for transplantation.
For now, however, the discovery is best viewed as an early but promising foundation for regenerative cardiology rather than an immediate treatment. By showing that human heart cells can respond to injury by producing new muscle cells, the research opens a new question for scientists: How can the heart’s natural repair process be strengthened enough to make a meaningful difference for patients?
