Washington, Dec 1 (ANI): Scientists from Imperial College London have identified a molecule that triggers damage in arteries, which causes heart attacks and strokes.
They hope that the condition could potentially be treated by blocking the molecule that triggers the damage.
The trigger identified in the research is a molecule called TLR-2. This 'receptor' molecule lives on the surface of an immune cell and when it recognises harmful molecules and cells, including bacteria, it switches the immune cell into attack mode, to protect the body.
It can also switch on the immune cells when the body is under stress.
The research team has shown that TLR-2 is unusually active in plaques in the carotid artery in the neck.
They showed blocking the TLR-2 receptor stopped cells from making the molecules that cause inflammation and damage to the artery in atherosclerosis.
This, they say, suggests that the molecule is triggering the damage to the artery. It also suggests that 'danger molecules,' which kick into action when the body is under stress, and bacteria, may be triggering damage to the arteries by switching on the TLR-2 molecules, increasing the risk of plaques bursting and causing strokes and heart attacks.
If a drug could be developed that would block TLR-2 molecules, the researchers believe this would potentially treat atherosclerosis and prevent damage to the artery.
They say this would ultimately reduce people's risk of strokes and heart attacks.
"Our new study reveals the trigger for inflammation and tissue breakdown in artery plaques," said Dr Claudia Monaco, one of the corresponding authors of the study from the Kennedy Institute of Rheumatology and Vascular Surgery at Imperial College London.
"We have also shown that this trigger mechanism can be blocked using antibodies. If we can find a way to successfully block these receptors in people, without reducing their ability to fight off infection, we could potentially develop a treatment for atherosclerosis," she added.
The research is published in the journal Circulation. (ANI)