Heart attacks and strokes remain two of the leading causes of death worldwide. Both conditions are often linked to a process called atherosclerosis, in which fatty deposits known as plaques build up inside the arteries.
Over time, these plaques can narrow blood vessels and reduce blood flow. However, doctors have long known that not all plaques are equally dangerous. Some plaques remain relatively stable for years, while others suddenly become unstable, rupture, and trigger blood clots that can block blood flow to the heart or brain.
A new study from researchers at The University of Texas MD Anderson Cancer Center has uncovered an important clue about why some plaques become so dangerous. The research, published in the journal Circulation Research, identified a molecular pathway that appears to drive inflammation and blood clot formation inside artery plaques.
The study focused on a special group of cells known as senescent cells. These are cells that have become stressed or aged. Unlike normal cells, senescent cells stop dividing, but they do not die and leave the body.
Instead, they remain in tissues and can influence nearby cells. Scientists have increasingly linked these aging cells to a wide range of diseases, including cancer, heart disease, and age-related disorders.
The research team wanted to understand how senescent cells affect blood vessels and plaque development. They focused on endothelial cells, which form the inner lining of blood vessels. Healthy endothelial cells help control blood flow and maintain stable blood vessel walls.
The scientists discovered that when two important proteins called LATS1 and LATS2 were lost, endothelial cells changed dramatically. Instead of remaining stable, they entered a senescent state but became unusually active.
These altered cells promoted inflammation, caused blood vessels to become leakier, encouraged abnormal blood vessel growth, and created conditions that favored blood clot formation.
Further investigation revealed that these changes were linked to a sharp increase in an enzyme called CD38. The enzyme appeared to reprogram how the cells produced and used energy. Rather than functioning normally, the cells consumed extra energy and shifted into a state that promoted inflammation and instability.
This process created an environment in which artery plaques became more vulnerable and more likely to develop blood clots. The researchers found that CD38 acted as a major driver of this harmful chain of events.
Importantly, when the scientists blocked CD38 activity, many of the harmful effects were reversed. In laboratory experiments and animal studies, inhibiting CD38 reduced inflammation and improved plaque stability. These findings suggest that CD38 may be a promising target for future treatments.
One particularly encouraging aspect of the study is that some drugs that target CD38 are already approved by the U.S. Food and Drug Administration for certain cancers. Because these medications already exist, researchers may be able to explore their potential use in cardiovascular disease more quickly than developing an entirely new drug from scratch.
The researchers also examined human plaque samples and found similar molecular patterns. This suggests that the biological mechanisms identified in the study may also occur in people, not just in laboratory models.
The findings may have additional importance for cancer patients. Many cancer treatments can accelerate cellular aging and increase the number of senescent cells in the body.
Some patients receiving cancer therapy experience higher rates of cardiovascular complications, including heart attacks, strokes, and blood vessel inflammation. The newly discovered pathway may help explain why these side effects occur.
According to the researchers, understanding how senescent cells influence blood vessel health could open new opportunities for preventing cardiovascular disease. By targeting the molecular processes that destabilize plaques, future therapies may help reduce the risk of life-threatening blood clots.
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Source: The University of Texas MD Anderson Cancer Center.
