An anti-ageing gene found in a population of centenarians has been shown to rewind the heart’s biological age by 10 years.
The research, led by scientists at the University of Bristol and the MultiMedica Group in Italy, demonstrates for the first time that a healthy gene could be transferred to unrelated people to protect their hearts.
Professor James Leiper, Associate Medical Director at the British Heart Foundation, which funded the research, said:
“We all want to know the secrets of ageing and how we might slow down age-related disease.
“Our heart function declines with age but this research has extraordinarily revealed that a variant of a gene that is commonly found in long-lived people can halt and even reverse ageing of the heart in mice.
“This is still early-stage research, but could one day provide a revolutionary way to treat people with heart failure and even stop the debilitating condition from developing in the first place.”
Carriers of healthy mutant genes, such as those living in blue zones of the planet, often live to 100 years or more, remaining in good health.
These individuals are also less prone to cardiovascular problems.
The researchers believe the gene helps to keep their hearts young by protecting them against diseases linked to ageing, such as heart failure.
In the new study, scientists demonstrate that one of these healthy mutant genes, previously proved particularly frequent in centenarians, can protect cells collected from patients with heart failure requiring cardiac transplantation.
The Bristol researchers discovered that a single administration of the mutant anti-ageing gene halted the decay of heart function in middle-aged mice.
And when given to elderly mice, whose hearts exhibit the same alterations observed in elderly patients, the gene was shown to rewind the heart’s biological clock age by the human equivalent of more than ten years.
The three-year study was also performed in test tube human cardiac cells by researchers in Italy.
A team from the MultiMedica Group in Milan administered the gene in heart cells from elderly patients with severe heart problems, including transplantation, and then compared their function with those of healthy people.
Monica Cattaneo, a researcher from the MultiMedica Group, said:
“The cells of the elderly patients, in particular those that support the construction of new blood vessels, called ‘pericytes’, were found to be less performing and more aged.
“By adding the longevity gene/protein to the test tube, we observed a process of cardiac rejuvenation: the cardiac cells of elderly heart failure patients have resumed functioning properly, proving to be more efficient in building new blood vessels.”
Professor Madeddu, Professor of Experimental Cardiovascular Medicine from Bristol Heart Institute at the University of Bristol, said:
“Our findings confirm the healthy mutant gene can reverse the decline of heart performance in older people.
“We are now interested in determining if giving the protein instead of the gene can also work.
“Gene therapy is widely used to treat diseases caused by bad genes. However, a treatment based on a protein is safer and more viable than gene therapy.”
