‘Centenarian gene’ found in humans who live longer than normal protects mice from developing heart disease in medical breakthrough
- Variation of the gene LAV has been found in people who live for a very long time
- Inserted gene into mice that were genetically vulnerable to heart disease
- Reduced amount of plaque in the rodents’ arteries, which raises blood pressure
The ‘centenarian gene’ could lead to the development of drugs that prevent heart attacks and strokes, research suggests.
Scientists found giving mice a variation of the gene LAV – found in humans who live for a very long time – protected them for atherosclerosis.
It slashed the amount of plaque in their arteries, known to raise blood pressure and can ‘break off’ to cause heart attacks or strokes.
The Italian researchers hope their study will ‘pave the way’ towards LAV treatments that ‘slow cardiovascular damage due to age’.
The ‘centenarian gene’ could lead to the development of ‘life-prolonging’ drugs (stock)
Atherosclerosis is a leading cause of heart disease, which is responsible for one in four deaths in the UK and US, statistics show.
It occurs when plaques made of fat, cholesterol, calcium and other substances accumulate in artery walls.
People who live for a long time have been found to ‘delay or escape atherosclerosis’, the researchers wrote in the European Heart Journal.
WHAT IS ATHEROSCLEROSIS?
Atherosclerosis occurs when plaques made of fat, cholesterol, calcium and other substances accumulate in artery walls.
Over time, the blood vessels harden and narrow, which restricts the flow of blood around the body.
When these plaques rupture, they form a blood clot that can further block the flow of oxygen-rich blood.
Atherosclerosis is most serious when it reduces blood supply to the heart or brain, which can result in a heart attack or stroke, respectively.
The condition, and the diseases it can cause, is the single biggest cause of death in the developed world, with it being responsible for one in three fatalities.
Atherosclerosis often starts in childhood and worsens with age, however, most do not experience symptoms until middle age or older.
Risk factors include:
- High blood pressure
- Elevated cholesterol levels
- Poor nutrition
- Excessive alcohol consumption
All the above can damage the thin layer, the endothelium, that keeps the inside of our arteries smooth.
Once damaged, ‘bad’ cholesterol accumulates in the artery wall.
The body sends immune cells to clean up this cholesterol, which can then get stuck in the damaged site.
This causes plaque to build-up over time.
Source: Heart Research Institute
Past research by the same scientists at the University of Salerno found long-living individuals express the LAV variant BPIFB4.
The researchers genetically engineered mice that were at risk of heart disease to express LAV-BPIFB4 or ‘normal’ LAV.
‘The results were extremely encouraging,’ lead author Dr Annibale Puca said.
‘We observed an improvement in the functionality of the endothelium (the inner surface of blood vessels).
‘[As well as] a reduction of atherosclerotic plaques in the arteries and a decrease in the inflammatory state.’
Narrowed or blocked blood vessels can lead to chest pain, heart attacks or strokes.
Inflammation may occur if the body recognises plaque in the arteries as a foreign substance and then launches an immune response against it.
Over time, this may irritate the blood vessels and loosen plaque, leading to embolisms.
This can further restrict the supply of oxygen-rich blood to the heart and brain.
In a second part of the experiment, the LAV-BPIFB4 was put into human blood vessels in the laboratory.
This produced ‘the same positive effect’, with LAV-BPIFB4 helping to create healthier blood vessels.
Study author Dr Carmine Vecchione said: ‘This paves the way to the possibility of therapeutic solutions based on LAV-BPIFB4 protein.
‘Of course, much research will still be needed.
But we think it is possible, by administering the protein to patients, to slow down cardiovascular damage due to age.
‘In other words, even if a person does not possess those particular genetic characteristics, we could be able to offer the same level of protection.’