Unregulated cell growth seems to be a driver behind the growth of atherosclerotic plaques, changing the traditional story of plaque formation. The rapid cell growth in the arterial wall is similar to pre-cancerous growth in other tissues.
For decades, the standard story of how atherosclerotic plaque forms focused on the accumulation of cholesterol and inflammatory cells in arterial walls. Now, researchers at the Stanford School of Medicine have identified another factor that initiates the formation of these plaques: inflamed smooth muscle cells in the linings of arterial walls that multiply in an unregulated way.
The culprit behind many heart attacks and strokes, atherosclerotic plaques are unhealthy masses of oxidized cholesterol, immune cells and dead tissue that form within arterial walls. When atherosclerotic plaques grow large or rupture they can impede blood supply to vital tissues and organs, making them a lethal threat.
“Cardiovascular disease remains the world’s No. 1 killer, despite widespread use of cholesterol-lowering medicines,” said Nicholas Leeper, MD, professor of surgery at Stanford. “Recent studies have indicated that the standard dogma about how atherosclerosis happens wasn’t really capturing the whole story.”
In 1973, researchers proposed that a substantial portion of atherosclerotic plaques were made up of arterial blood vessel cells that had expanded over time, and that these abnormally growing cells could be driving the growth of the plaque. But for decades, that idea was sidelined in favor of findings pointing to the importance of cholesterol in plaque formation.