
Researchers at King’s College London have for the first time highlighted the natural regenerative capacity of a group of stem cells that reside in the heart.
This new study shows that these cells are responsible for repairing and regenerating muscle tissue damaged by a heart attack which leads to heart failure.
The study, published today in the journal Cell, shows that if the stem cells are eliminated, the heart is unable to repair after damage. If the cardiac stem cells are replaced the heart repairs itself, leading to complete cellular, anatomical and functional heart recovery, with the heart returning to normal and pumping at a regular rate.
Also, if the cardiac stem cells are removed and re-injected, they naturally ‘home’ to and repair the damaged heart, a discovery that could lead to less-invasive treatments and even early prevention of heart failure in the future.
The study, funded by the European Commission Seventh Framework Programme (FP7), set out to establish the role of cardiac stem cells (eCSCs) by first removing the cells from the hearts of rodents with heart failure. This stopped regeneration and recovery of the heart, demonstrating the intrinsic regenerative capacity of these cells for repairing the heart in response to heart failure.
Heart failure – when the heart is unable to pump blood around the body adequately – affects more than 750,000 people in the UK, causing breathlessness and impeding daily activities. Current treatments are aimed at treating the underlying causes, such as coronary heart disease, heart attack and blood pressure through lifestyle changes, medicines and in severe cases, surgery. These treatments are sometimes successful in preventing or delaying heart failure. However, once heart failure develops the only curative treatment is heart transplantation.
By revealing this robust homing mechanism, which causes cardiac stem cells to home to and repair the heart’s damaged muscle, the findings could lead to less invasive treatments or even preventative measures aimed at maintaining or increasing the activity of the heart’s own cardiac stem cells.
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