Researchers from Italy and the UK we found a gene in a population of centenarians can delay biological age by 10 years which could represent a significant advance for patients with heart failure.
A series of positive attributes have been identified in long-lived people, such as do not smoke tobacco, eat a healthy diet, perform regular physical activityavoiding stress, and having a positive outlook on life, but the presence of this gene could be key to helping others.
This study was led by scientists from the University of Bristol and Italy’s MultiMedica Group and was published in the journal Cardiovascular Research.
Carriers of these mutant genes live 100 years or more in good health. and are less prone to cardiovascular complications. Therein lies a therapeutic possibility for patients with heart failure.
The researchers, funded by the British Heart Foundation, believe that the gene helps keep their hearts young by protecting them against aging-related diseases, like heart failure. In this new study, the researchers showed that one of these healthy mutant genes, which until now had been shown to be especially prevalent in centenarians, it may protect cells taken from heart failure patients requiring heart transplantation.
According to Paolo Madeddu, a professor leading the Bristol team, a single administration of the mutant anti-aging gene halted the decline in heart function in middle-aged mice.
Madeddu, Professor of Experimental Cardiovascular Medicine at the University of Bristol Heart Institute, explained: “The functioning of the heart and blood vessels come into play as we age. However, the rate at which these damaging changes occur varies from person to person.”
The cigarette, the alcohol, the sedentary life condition the functioning of the heart, but also genetics designs the way in which each person will age and it is in this field where science can intervene.
“Genes are sequences of letters that code for proteins. By chance, some of those letters may change. Most of these changes are insignificant; in a few cases. However, the mutation can worsen or improve the function of the gene, as in the case of the mutant anti-aging gene that we have studied here in human cells and old mice”, explained the scientist.
This research has been going on for the last three years and was carried out on human heart cells in the laboratory in Italy. Annibale Puca, director of the MultiMedica group in Milan, said they administered the gene into heart cells from elderly patients with severe heart problems, including transplantation, and then compared its performance with healthy individuals.
Monica Cattaneo, a researcher at the MultiMedica Group in Milan, Italy, explained that “the cells of elderly patients, particularly those that promote the construction of new blood vessels, are called pericytes.” These may age and become less effective, but “by adding the longevity gene/protein to the test tube, we observed a cardiac rejuvenation process: heart cells from older heart failure patients returned to function properly, proving to be more effective.” in the construction of new blood vessels”, said Cattaneo.
Treatments for children
Professor Madeddu added: “Our findings confirm that the healthy mutant gene can reverse the decline in cardiac performance in older people. Now we are interested in determining if giving the protein instead of the gene can also work”, since a treatment based on a protein could be safer and more feasible.
“We have received funding from the Medical Research Council to test healthy gene therapy in progeria. This genetic disease, also known as Hutchinson-Gilford syndrome, causes premature aging damage to the heart and blood vessels of children. We have also been funded by the British Heart Foundation and Diabetes UK to test the protein in elderly and diabetic mice respectively,” she announced.
From the study that was published in Cardiovascular Research, there is “new confirmation and expansion of the therapeutic potential of the gene/protein. We hope to soon test its efficacy in clinical trials with patients with heart failure”, concluded Puca.
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