Cancer-Like Proliferation of Smooth Muscle Cells in Atherosclerosis
Atherosclerosis, a leading cause of heart attacks and strokes, involves the buildup of fat deposits in arteries. Recent research has unveiled a concerning similarity between the behavior of smooth muscle cells in atherosclerotic plaques and cancerous cells. These smooth muscle cells undergo significant changes, proliferate rapidly, and contribute to the growth of fatty plaques that can rupture and lead to severe cardiovascular events. Further investigations have revealed DNA damage in these cells, reminiscent of cancer, which accelerates atherosclerosis progression. The implications of these findings suggest that anticancer therapies may hold promise in treating or preventing atherosclerosis.
Previous studies had observed the transformation of smooth muscle cells within atherosclerotic plaques, with these cells multiplying and taking on diverse roles in the plaque composition. However, the resemblance to cancer cells and its impact on atherosclerosis had not been thoroughly explored until now. By closely monitoring the behavior of transformed smooth muscle cells in both mouse models and human plaques, researchers identified similarities between these altered cells and cancer cells, including enhanced proliferation, resistance to cell death, and invasiveness. The accumulation of DNA damage in these cells was a key finding, suggesting a potential driver of atherosclerosis development. Manipulating DNA damage levels in smooth muscle cells further exacerbated atherosclerosis in mice, underscoring the significance of this cell behavior in disease progression.
This groundbreaking research opens the door to new therapeutic avenues for atherosclerosis, hinting at the possibility of leveraging existing anticancer strategies to combat the disease. Further exploration in human subjects and animal models is necessary to validate these findings and explore the full potential of targeting cancer-like cells in atherosclerosis treatment. For more details, you can access the original news release here.
