Human Heart Muscle Regrows After Heart Attack, Study Finds — SkimNews

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- University of Sydney researchers, working with the Baird Institute and Royal Prince Alfred Hospital, demonstrated for the first time that human heart muscle cells regenerate after a heart attack — overturning the long-held belief that lost heart muscle cannot be replaced.
- First author Dr. Robert Hume, of the Faculty of Medicine and Health and Charles Perkins Centre, said the heart is left scarred after an attack but also produces new muscle cells, though not enough to replace all tissue lost — a single heart attack can destroy up to one-third of the heart's cells.
- Senior author Professor Sean Lal, a heart failure cardiologist at Royal Prince Alfred Hospital, said the team's goal is to develop therapies that make new heart cells to reverse heart failure, and that researchers have already identified several proteins linked to regeneration previously observed only in mice.
- The study relied on a world-first technique using living "pre-mortem" heart tissue collected from consenting bypass surgery patients at Royal Prince Alfred Hospital, developed jointly by Professors Paul Bannon and Sean Lal.
- The findings were published in Circulation Research and directly extend prior mouse studies showing increased cell division in heart muscle after infarction — making this the first confirmation of the same regenerative response in humans.
- Cardiovascular disease causes roughly 24% of all deaths in Australia, where approximately 144,000 people live with heart failure but only about 115 heart transplants are performed each year — a gap that underscores why an alternative to transplantation is urgently needed.
Why it matters: A heart transplant is the only cure for heart failure, yet Australia performs only about 115 per year against roughly 144,000 patients living with the condition, leaving the vast majority dependent on palliative management. Confirming that the adult human heart retains any regenerative capacity at all gives researchers a concrete biological target that does not depend on scarce donor organs.
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