Newcastle University scientists are killing zombie cells to reverse age-related damage in the heart

8 February 2019        

Category: Research

New research published today from a team at Newcastle University, shows it may be possible to reverse the damage in the heart caused by ageing.

An illustration of zombies.'Zombie cells' are cells that are damaged - but not dead - and can cause other cells around them to become zombified...

We part-funded the study, the findings of which were published in the European Molecular Biology Organisation (EMBO) Journal. The paper suggests a new way of preventing heart failure in older patients.

Zombies exist, but maybe not where you'd expect them...

Heart failure occurs when the heart is not pumping blood around the body as well as it should, most commonly when the heart muscle has been damaged – for example, after a heart attack. More than 580,000 people in the UK are on their GP’s heart failure register.

Ageing is one of the main risk-factors for heart failure, as older people are more likely to develop heart disease and don’t recover as well following a heart attack.

This research, led by Dr João Passos, Dr Jeanne Mialet-Perez and Dr Gavin Richardson, explores how senescent cells – also known as zombie cells – form in the heart during ageing and lead to heart failure.

Zombie cells occur all over the body as it ages. They get their nickname from the fact that although they are not dead they do not function correctly and can cause other cells around them to become senescent (or zombiefied!)

Elsewhere in the body, zombie cells are usually caused by the shortening of structures found at the end of chromosomes called telomeres, which happens progressively each time a cell divides. But as heart cells – cardiomyocytes – rarely divide it was not known if or how these cells could become senescent.

A greater understanding of how cells age

A montage of two images taken with a microscope, showing mitochondria (red) and telomeres (green) in an embryonic heart muscle cell.A montage of two images taken with a microscope, showing mitochondria (red) and telomeres (green) in an embryonic heart muscle cell.

The Newcastle scientists, in collaboration with researchers in the Mayo Clinic in the US and Inserm in France have not only discovered how this process takes place in the heart but also how it can be reversed or treated.

“Previously, it was believed that senescence occurs only as a result of a lifetime of cell division and the shortening of telomeres. Our data support the very exciting idea that heart cells can become senescent due to stress that damages their telomeres rather than the process of division,” said Dr Passos. “This mechanism could also explain how other non-dividing cells in our bodies age.”

A door to new treatments

“We saw that removing senescent cardiomyocytes from the hearts of aged mice, both genetically and using drugs, was able to restore cardiac health – essentially removing the damage caused by ageing. This data provides critical support for the potential of using medicines to kill zombie cells. If this is validated through clinical trials it would provide us with a new way of treating cardiac diseases,” explained Dr Richardson.

Based on this research, the team are now exploring the effects of removing senescent cells found as a consequence of a heart attack.

Our Associate Medical Director Jeremy Pearson said “People are living longer lives, but often as they get older, their health deteriorates and their quality of life is negatively affected. This research is exciting because it could potentially help us to tackle the increasing numbers of people with heart failure, meaning that older people could stay well for longer, and continue to lead full and active lives. The research is still in its early stages, but this study funded in part by the generous donations of our supporters could be the first step towards a new era for healthy ageing.”

This research was made possible via a BHF project grant of £295,743, awarded to the Newcastle University team in February 2016. We can only continue to support incredible research with the generous donations of our supporters. To find out more about supporting our life saving work, visit