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Headlines Published on 29 December 2006

Title EU-funded research identifies mechanism leading to heart attack, stroke

The opening lecture at the third conference of European Vascular Genomics Network (EVGN) was the setting for the release of promising new research in cardiovascular research. Graciela B. Sala-Newby presented members of EVGN, the first European Union Network of Excellence for cardiovascular disease, the findings of her research regarding the development and behaviour of foam cells (FCM) and the role they have to play in stroke and heart attacks.

Naturally occurring macrophages may be responsible for tiny fragments in the blood which lead to stroke. © Matt+
Naturally occurring macrophages may be responsible for tiny fragments in the blood which lead to stroke.
Cardiovascular diseases (CVDs) are attracting more and more attention from EU health officials as the number of cases attributed to them are on the rise. Currently, CVDs are responsible for more deaths than cancer, which is often mistakenly considered the most malignant condition in industrialised countries. Every year, the affects of CVDs, such as stroke and heart attacks, are responsible for 5 million deaths in Europe, and cost, directly or indirectly, the European economy approximately €3 billion. The fact that CVDs are behind about 50 percent of all deaths in Europe makes Dr Sala-Newby’s discoveries all the more relevant.

Atherosclerosis is a CVD that leads to the hardening of arterial walls. It is caused by plaques which build up along the inside of the arteries restricting blood flow. As atherosclerosis develops, plaque can become unstable and release tiny fragments, or thrombi, into the blood stream. These fragments can make their way into the blood vessels of the heart or brain blocking critical blood flow, which in turn leads to heart attack or stroke.

Dr Sala-Newby and her research team from Bristol Heart Institute, University of Bristol believe they have uncovered the genetic root of the processes that lead to the destabilisation of plaques in the arteries. They expect the research to lead to new perspectives for the treatment of atherosclerosis, suggesting novel targets to slow down and possibly prevent plaque rupture.

The body’s natural defences produce a layer of connective tissue on the plaque that develops in arteries, however they can also cause pieces to become dislodged, producing the dangerous thrombi. Dr Sla-Newby was looking for the trigger that causes the instability of the plaques, and may have found it in foam cells.

“We hypothesised that the conversion of macrophages (white blood cells) into foam cells could be due to genetic changes that up- or down- regulate the amount of proteins produced within these cells,” explains Dr Sala-Newby.

Through laboratory testing, Dr Sala-Newby and her team are confident they have found the genes that cause the transformation they were looking for. The team plans to focus on one gene in particular, one which produces the enzyme Metalloproteinase-12 (MMP-12), as a candidate for producing future therapies.

“MMP-12 is particularly abundant in the deeper layers of the plaques, and its presence strongly correlates with their instability. Finding the way to inhibit its production would give us a useful tool to counteract plaque rupture.”

More information:

  • European Vascular Genomics Network (EVGN)
  • Life sciences, genomics and biotechnology for health

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