The long-held belief among doctors is that smooth muscle cells only interaction with build-ups in blood vessels was to attempt to keep them from moving. It turns out the cells contribute to their growth and progression as well. Photo: Designua/Shutterstock

CHARLOTTESVILLE, Va., July 6 (UPI) -- Researchers have found that one of the basic understandings of atherosclerosis -- that smooth muscle cells which help blood vessels operate act to prevent plaques inside of them from dislodging -- is at least partially incorrect, which may cause shifts in the way that doctors treat the disease.

Smooth muscle cells have been thought to "wall off" plaques as a defense mechanism on the part of the body, however researchers found that plaques actually contain many of the these cells which may in some cases make the plaques worse.


Researchers discovered that there were far more of the cells contributing to the buildup of plaques than there are walling off the collection fats, dying cells and other components.

"We suspected there was a small number of smooth muscle cells we were failing to identify using the typical immunostaining detection methods. It wasn't a small number. It was 82 percent," said Gary Owens, Ph.D., of the University of Virginia's Robert M. Berne Cardiovascular Research Center, in a press release.

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"Eighty-two percent of the smooth muscle cells within advanced atherosclerotic lesions cannot be identified using the typical methodology since the lesion cells down-regulate smooth muscle cell markers. As such, we have grossly underestimated how many smooth muscle cells are in the lesion."

Researchers made the discovery in a recent study by genetically tagging young smooth muscle cells. As they watched atherosclerosis progress in mice, they were able to mark the cells more easily because of the tagging, however they discovered the cells are often disguised within the legion and difficult to distinguish.

During the study, they also identified a gene, Klf4, that appeared to regulate transitions smooth muscle cells make inside of the legions. When researchers turned this gene off, they saw the athersclerotic plaques shrink "dramatically." While the number of cells present in them was not necessarily decreased, their effect at making the problem worse appeared to be mitigated.

"The leading cause of death worldwide is complications of atherosclerosis, and the most common end-stage disease is when an atherosclerotic plaque ruptures. If this occurs in one of your large coronary arteries, it's a catastrophic event," Owens said. "As such, understanding what controls the stability of plaques is extremely important."

The study is published in Nature Medicine.