The researchers observed significant DNA damage and rapid cell growth in both human and mouse arteries affected by atherosclerosis. “DNA damage is one of the major features of cancer,” said Dr. Pan.
These SMCs displayed several cancer-like traits—they multiplied rapidly, resisted cell death, invaded surrounding areas, and showed increased DNA damage. This DNA damage, typically absent in healthy arteries, was common in atherosclerotic plaques and appeared to worsen the disease. The treatment significantly reduced the size of the plaques and made them more stable.
Stable plaques are less likely to rupture, which can prevent serious cardiovascular events like heart attacks and strokes. Unstable plaques can break apart and block blood flow, leading to these life-threatening conditions. The study authors suggest that their research opens the door for further investigation into the cancer-like behavior of atherosclerosis.
By identifying specific mutations and understanding DNA damage in patients, doctors could develop personalized therapies. According to the authors, the broader concept, called “athero-oncology,” suggests that cancer treatments might revolutionize the treatment of atherosclerosis. “If considering implications for human disease treatment, more pre-clinical work needs to be done, such as testing for side effects, deeper studies on how it works in atherosclerosis, and whether it influences other diseases,” Dr.
Pan said. Dr. Pan acknowledges this, stating.