Scientists have identified a genetic mechanism which appears to determine which fatty deposits in the arteries have the potential to kill us.
- Most of these plaques pose no risk to health, but a minority burst, forming blood clots, which can cause heart attacks or strokes.
- A Columbia University team pinpointed a gene which seems to make plaques more vulnerable to rupture.
- The American study appears in the journal Cell Metabolism.
- Fatty deposits begin to form in the arteries of most people in their teens, but the vast majority are harmless.
- However, it is thought that around 2% of plaques have the potential to burst.
- This can lead to the development of a clot, which can restrict blood supply to the heart or brain, with potentially grave consequences. Scientists believe one of the key factors determining whether a plaque will burst is the make up of its inner core.
- The inner core of plaques vulnerable to rupture often contains a lot of dead cells.These cells release substances that can weaken the surface cap of the plaque, making rupture more likely.
- The researchers bred mice prone to develop plaques, and fed them a high-fat diet for 10 weeks.The animals which lacked the key gene tended to produce smaller plaques, and to show markedly lower levels of cell death and plaque degradation.
- The gene in question produces a protein which plays a central role in a mechanism used by the body to kill off cells that are damaged and unhealthy.
- But there is some evidence to suggest that the process may sometimes become too aggressive, and may lead to problems such as neurodegenerative diseases and diabetes.
- He said: "The fact that we were able to isolate one gene encoding one protein with such a profound effect on plaque necrosis (death) was a big surprise."
- "Just about everybody in our society has atherosclerosis (thickening of the arteries) by the time we reach 20," he said.
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