When fats, immune cells, connective tissue, and debris build up inside the arteries—forming atherosclerotic plaques—they boost a person’s risk of heart attack or stroke. Now, researchers led by Daniel Greif, MD, associate professor of medicine and genetics, have followed the role of smooth muscle cells in forming those plaques.
While multiple smooth muscle cell progenitors give rise to arterial walls during development, the researchers determined in mouse models that rare smooth muscle cell progenitors contribute to plaques. Greif’s team found that these “cap cells” made their way to the center of a plaque and altered the nature of the surrounding environment, encouraging inflammation and further plaque growth.
The full chain of events, which the researchers described on May 25 in Nature Communications, can initially depend on the presence of a gene known as integrin beta3 (Itgb3). When mice lacked Itgb3, smooth muscle cells were found to be more likely to move aggressively into plaques.
The research points toward the smooth muscle cell-derived cap cells, and integrin beta3, as potential targets for atherosclerosis therapy that warrant “intense investigation.”