Scientists find the enzyme responsible for increasing the risk of developing coronary heart disease, which can lead to new treatments, reports Medical Xpress.
An enzyme named ADAMTS7 has been found, which is beleived to be reponsible for developing coronary heart disease. It helps in building up the cells in the coronary arteries and narrowing them down. Eventually, blood supply to the heart is blocked by the fat deposited in the walls of coronary arteries, says the report. These fatty deposits blocking the bloody supply to the heart are called atherosclerotic plaques.
The deadly disease is often caused due to smoking cigarettes, unhealthy diet and lack of exercise killing more than 94,000 people in the U.K. every year.
"Recent studies have identified a number of genetic regions that are associated with coronary heart disease," says research lead, Shu Ye, professor of Molecular Medicine and Genetics at Queen Mary, University of London, reports Medical Xpress. "However, to translate these findings into new therapeutics which could benefit patients, we need to understand how these genetic variants are influencing the disease."
Scientists mainly focused on the genetic region linked to coronary heart disease and also contained the ADAMTS7 gene. The function of ADAMTS7 was monitored closely and was found that it produces an enzyme which is also named ADAMTS7 which crashes thrombospondin-5, a structural protein in the coronary arterial wall, that leads to free movement of the cells in the wall. The free movement of the cells in the arterial wall drifts towards the atherosclerotic plaques which increases their size and narrows down the artery, according to the report.
"Through analysing arterial cells from 18 individuals, we found that this ADAMTS7 gene variant reduces the ability of the ADAMTS7 enzyme to break down the structural protein thrombospondin-5," Professor Ye added. "As a result, arterial cells are less able to migrate and consequently we found that individuals carrying this genetic variant are less likely to develop atherosclerotic plaques and, even if they do, the plaques tend to be smaller. Further research is needed but this indicates that ADAMTS7 would be a promising target against which new medicines could be designed to act."
The findings are published online in The American Journal of Human Genetics.
