The researchers revealed that the mysterious mechanism of hardening of the arteries may have been resolved, also suggesting the first potential preventative drug in the treatment of heart attack, dementia, and stroke.
Arteries harden as calcium is deposited in the elastic walls of vessels, a process that occurs with age and is exacerbated for patients with diabetes or kidney disease. Stiffening can also occur when calcium is deposited in the fatty tissue of the arteries – a condition called atherosclerosis.
The mechanism that causes calcium deposition has been difficult to take off, but scientists now say it has the answer: it is triggered by a molecule, called poly (ADP-Ribose) or PAR, which is produced when cells, or DNA inside, are damaged.
This makes sense: aging, high blood pressure, smoking and fat plaques are risk factors for stiffening the arteries and are linked to cell damage, or even their DNA.
The team says the new discovery could prove important for patients.
"Yes [the calcification process] is guided by cells, which means you can actually treat it, "said Cathy Shanahan, professor of cell signaling and co-author of the study at King's College London.
In the journal Cell Reports, the team describes a series of experiments involving bone-forming tissues from sheep and blood vessel cells from cows, as well as human arteries.
The results reveal that where PAR is at high concentrations outside cells, calcium deposits are also present. In addition, these regions have been shown to be rich in markers of cell death or in cells damaged by DNA.
They also discovered that PAR binds to calcium, as well as to certain proteins found between the cells of artery walls and bone-forming tissues.
As a result, the team proposes that PAR, which has previously been associated with DNA repair and cell death, plays a key role not only in bone formation, but also in the hardening of bone. arteries.
Crucially, other experiments, including in the rat, have shown that if an enzyme involved in the production of PAR is blocked, calcium is no longer deposited in the arteries, even when the DNA is damaged. They also discovered that an antibiotic already used against acne, minocycline, could do the job.
"People have been studying this for decades and it's the first potential therapy of all time," said Professor Melinda Duer, co-author of the University of Cambridge study.
However, the team says that although some risk groups could be prevented from stiffening the arteries, questions remain.
Duer pointed out that individuals should continue to avoid lifestyle habits that could contribute to stiffening arteries, including smoking and poor nutrition.
Shanahan agreed. "What we do not know is if it will work for people who already have a lot of calcification," she said.
Paul Evans, a professor of cardiovascular sciences at the University of Sheffield, said that drugs such as minocycline, which stop the production of PAR, could one day help patients with arterial disease.
"There is considerable interest in the development of PAR inhibitors for cancer and other diseases," he said. "It is possible that some of these drugs may benefit patients with cardiovascular disease by alleviating the symptoms of angina and reducing the risk of heart attack or stroke."