Columbia University researchers have discovered that cells found inside clogged arteries have similar properties to cancer cells, which can worsen atherosclerosis. This raises the potential for using anticancer drugs as a new form of treatment for atherosclerosis and to help prevent heart attacks. The study found that the smooth muscle cells that typically line the interior of our arteries migrate into the plaques caused by atherosclerosis and undergo changes that activate cancer-like characteristics.The research indicates that the modified muscle cells are responsible for the development of atherosclerosis, which could lead to new treatment options for the disease. Muredach Reilly, MD, the Florence and Herbert Irving Endowed Professor of Medicine at Columbia University Vagelos College of Physicians and Surgeons and director of Columbia’s Irving Institute for Clinical and Translational Research, suggests that existing cancer drugs may potentially be used to treat atherosclerosis. The study, which was published in Circulation on April 30, was conducted by Reilly and Huize Pan, who is currently an assistant professor of medicine at Vanderbilt University Medical Center.The study was conducted by Dr. Ian J. Korf, who was an associate research scientist at Columbia at the time.
DNA damage and hyperproliferation
Atherosclerosis is a leading cause of heart attacks and stroke globally, occurring when fatty deposits accumulate inside the arteries. Atherosclerosis can be mitigated with a healthy diet or statin drugs, which slow down or reverse the buildup of deposits.
Prior research had indicated that smooth muscle cells undergo a transformation into various cell types within these atherosclerotic plaques and proliferate to form the majority of cells within the plaques.
Research has investigated the cancer-like characteristics of cells and their potential contribution to atherosclerosis. Reilly and Pan closely monitored the transformation of smooth muscle cells in mice with atherosclerosis and examined plaques from individuals with the condition to gain further insights.
They discovered significant similarities between changes in smooth muscle cells and cancer cells, such as excessive cell growth, resistance to cell death, and invasiveness.
The accumulation of DNA damage, a hallmark of cancer, was observed in both mouse and human smooth muscle cells, and it seems to accelerate the progression of atherosclerosis, according to the researchers. They were able to establish a connection between the two through their findings.The researchers discovered that they could further speed up the development of atherosclerosis in mice by causing a genetic mutation that led to increased DNA damage in the smooth muscle cells. Healthy mice and humans did not show any signs of smooth muscle cells with the same DNA damage found in atherosclerotic plaques.
Additionally, the researchers did not find any evidence of the cancer spreading to other parts of the body. According to Reilly, the cells stayed within the existing plaques, leading the researchers to believe that they mostly behave like benign tumor cells. However, more research needs to be done in both humans and animal models to confirm this hypothesis.
The researchers are considering treating atherosclerosis similar to the way cancer is treated.Anticancer therapies, like cells, may offer a new potential approach to treating or preventing the disease.
Scientists studied this idea by using a common cancer drug, niraparib, on atherosclerotic mice. This drug targets cells with DNA damage. The results showed that the drug significantly reduced the size of the atherosclerotic plaques and improved plaque stability (which reduces the risk of heart attack).
“This indicates that cancer drugs such as niraparib could potentially prevent the buildup of plaques and also treat atherosclerosis once it has developed,” Reilly explains. “It’s important to note, however, that the experiment withniraparib demonstrated a principle but does not directly apply to clinical use. Other cancer medications may also have potential benefits. “We still need more research to identify the most effective targets, safest targeted treatments, and vascular delivery methods,” says Reilly. “We also need to determine if individuals have different types of DNA damage and mutations that contribute to the disease, and if so, we can utilize that information to create personalized therapies for atherosclerosis,” Reilly adds. “While statins are highly effective for many individuals in reducing atherosclerosis and preventing heart attacks, some people still experience significant cardiovascular issues.”At risk. Further investigation into the cancer-like characteristics of atherosclerosis is expected to result in new therapeutic options for these individuals.”
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