'Longevity gene' could reverse damage from rapid aging disease


Thursday, 23 October, 2025


'Longevity gene' could reverse damage from rapid aging disease

Researchers have found that a so-called ‘longevity gene’, found in people who live exceptionally long lives, could counteract the cardiovascular damage caused by the rare genetic disease known as progeria, which causes children to age rapidly. The research, by the University of Bristol and IRCCS MultiMedica, has been published in the journal Signal Transduction and Targeted Therapy.

Progeria, also known as Hutchinson–Gilford progeria syndrome (HGPS), is caused by a mutation in the LMNA gene, which leads to the production of a toxic protein called progerin. Progerin damages cells by disrupting the structure of their nucleus — the ‘control centre’ of the cell — leading to early signs of aging, especially in the heart and blood vessels. Most affected individuals die in their teens due to heart problems, although a few have lived longer (the oldest known person with progeria, Sammy Basso, died last year at the age of 28).

Currently, the only FDA-approved treatment for progeria is a drug called lonafarnib, which helps reduce the build-up of progerin. A newer clinical trial is now testing lonafarnib in combination with another drug called Progerinin to see if the combination works better.

In the new study, researchers sought to explore whether genes from supercentenarians (people who live to 110 or older) could help protect children with progeria from the damaging effects of progerin. The team focused on a gene called LAV-BPIFB4, which has previously been shown to help keep the heart and blood vessels healthy during aging.

Using animal mice models genetically engineered to have progeria, the research team were able to show early heart problems like those seen in children with the disease. The team found a single injection of the longevity gene helped improve heart function, specifically how the heart relaxes and fills with blood — called diastolic function.

The gene reduced heart tissue damage — called fibrosis — and decreased the number of ‘aged’ cells in the heart. The gene also boosted the growth of new small blood vessels, which could help keep heart tissue healthy.

The team then tested the effect of the longevity gene in human cells from progeria patients. Their findings showed adding the longevity gene to these cells reduced signs of aging and fibrosis, without changing progerin levels directly. This suggests the gene helps protect cells from the effects of progerin, rather than removing it. Importantly, the treatment doesn’t try to eliminate progerin but instead helps the body cope with its toxic effects.

“Our research has identified a protective effect of a ‘supercentenarian longevity gene’ against progeria heart dysfunction in both animal and cell models,” said Dr Yan Qiu, an Honorary Research Fellow in the Bristol Heart Institute at the University of Bristol.

“The results offer hope to a new type of therapy for progeria; one based on the natural biology of healthy aging rather than blocking the faulty protein. This approach, in time, could also help fight normal age-related heart disease.”

Professor Annibale Puca, Research Group Leader at IRCCS MultiMedica and Dean of the Faculty of Medicine at the University of Salerno, added: “This is the first study to indicate that a longevity-associated gene can counteract the cardiovascular damage caused by progeria.

“The results pave the way for new treatment strategies for this rare disease, which urgently requires innovative cardiovascular drugs capable of improving both long-term survival and patient quality of life. Looking ahead, the administration of the LAV-BPIFB4 gene through gene therapy could be replaced and/or complemented by new protein- or RNA-based delivery methods.

“We are currently conducting numerous studies to investigate the potential of LAV-BPIFB4 in counteracting the deterioration of the cardiovascular and immune systems in various pathological conditions, with the goal of translating these experimental findings into a new biologic drug.”

Image credit: Progeria Research Foundation.

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