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The depositing of calcium, or calcification, helps to harden tissues in the body. Tissue hardening is essential for healthy bone development, but it can cause health problems when it occurs in arteries.

Stiff, or hard, arteries impede the flow of nourishing blood to tissues and organs. This can raise the risk of cardiovascular conditions, such as high blood pressure, heart attack, and stroke. It can also raise the risk of dementia and other age-related diseases.

Now, scientists at the University of Cambridge and King’s College London, both in the United Kingdom, have unraveled the chemical changes that cause arteries to harden.

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The study centers around a molecule called PAR, which is short for poly(ADP-ribose). The researchers discovered that PAR could form “dense liquid droplets with calcium ions, ” which then crystallize when they combine with the elastic tissues in artery walls.

Before the discovery, scientists thought that PAR only had a role in DNA repair. The new findings reveal that it also promotes calcification in arteries.

“Artery hardening happens to everyone as they age, ” says Melinda J. Duer, who is a professor in the Department of Chemistry at Cambridge University, “and is accelerated in patients on dialysis, where even children develop calcified arteries.”

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Duer co-led the study with Catherine M. Shanahan, who is a professor of cell signaling at King’s College London. They have been investigating artery calcification for more than 10 years.

In their study paper, the authors explain that calcification that hardens arteries commonly occurs at two sites in the blood vessel. One site is the intima, or the tissue that lines the blood vessel wall. Calcification at this site occurs as part of atherosclerosis.

The other site at which artery hardening occurs is in the media, or the tissue inside the blood vessel wall. Hardening of the media usually happens during aging.

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Shanahan explains that for this particular study, they wanted to find out what triggers the calcification, which takes the form of calcium phosphate crystals.

They were particularly interested in finding out why the deposits seem to concentrate “around the collagen and elastin, which makes up much of the artery wall.”

In earlier work, the teams had discovered that PAR, which carries out DNA repair inside cells, can also operate outside of cells as a driver of bone tissue production.

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Also, when cells undergo oxidative stress and DNA damage, they express two enzymes that produce PAR — PARP1 and PARP2. Scientists have often seen that oxidative stress and DNA damage can accompany calcification in bone and blood vessels.

They found that as cells perish from oxidative stress, they export PAR. Because PAR has a strong affinity to calcium ions, once it is outside of the cell, it attaches firmly to calcium in preference to other minerals.

This process produces large calcium droplets that attach to collagen and elastin, the materials in artery walls that give the vessels their elasticity. When the droplets attach to the elastic materials, they solidify into crystals, reducing elasticity and stiffening the arteries.

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Duer says that they made this discovery by accident at first and then pursued it. “We never would have predicted that it was caused by PAR, ” she notes.

Having established the role of PAR in artery calcification, the teams then went in search of a way to stop it. The obvious solution was to look for a PARP inhibitor, which is a molecule that blocks PAR production by blocking one of the enzymes that synthesizes it.

They decided to search for a PARP inhibitor among drugs that had already undergone trials in humans as this would shorten the development time for its use as a treatment to prevent stiff arteries.

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With the help of Cycle Pharmaceuticals, the researchers identified and tested six molecules that fit their criteria. One of these, minocycline, proved to be very effective at stopping arteries from becoming stiff in rats with long-term kidney disease.

Prof. Jeremy Pearson, Associate Medical Director at BHF, says that the researchers have revealed the mechanism behind artery calcification and also shown how it differs from bone calcification.

“By doing so, he adds, “they have been able to identify a potential treatment to reduce blood vessel calcification without any adverse effects on bone.”

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“ This type of treatment would benefit many people, and we eagerly await the results of the anticipated clinical trials looking at whether this drug lives up to its early promise.” Prof. Jeremy Pearson