Scientists discovered how slow-moving blood in curved arteries damages the cells that line blood vessels, leading to heart disease. When blood moves slowly through certain parts of arteries, it triggers a special type of cell death called ferroptosis in the endothelial cells (the protective lining of blood vessels). This process is controlled by a protein called P53, which normally protects our cells. In this study, researchers used mice and human cells to show that blocking this harmful process could prevent artery damage and plaque buildup. This finding could lead to new treatments for heart disease by stopping the cell damage before it starts.

The Quick Take

  • What they studied: How slow blood flow in curved parts of arteries damages the protective cells lining blood vessels and causes heart disease
  • Who participated: Male mice that were genetically prone to heart disease and fed a high-fat diet, plus human blood vessel cells grown in laboratory dishes
  • Key finding: Slow blood flow triggers a damaging process in artery-lining cells that leads to plaque buildup. Blocking this process with special drugs or genetic changes prevented artery damage in mice
  • What it means for you: This research suggests new ways to prevent heart disease by stopping cell damage in arteries before plaques form. However, these findings are from animal and lab studies, so human treatments are still years away

The Research Details

Researchers used two approaches to study how slow blood flow damages arteries. First, they used mice that naturally develop heart disease and partially blocked blood flow in one of their neck arteries to create areas of slow-moving blood. They fed these mice a high-fat diet to make the problem worse. Second, they grew human blood vessel cells in special laboratory dishes and used a device that simulates slow blood flow over these cells. This two-pronged approach allowed them to study the problem both in living animals and in controlled laboratory conditions.

The researchers then tested whether blocking the harmful cell death process (ferroptosis) could prevent artery damage. They used two methods: a drug called Fer-1 that stops ferroptosis, and genetic engineering to boost a protective protein called GPX4 in the mice’s blood vessel cells. They also tested what happened when they removed or blocked the P53 protein, which appears to control the entire damaging process.

Understanding exactly how slow blood flow causes artery damage is crucial because it happens in the same curved and branching areas where heart disease typically develops in humans. By identifying the specific molecular pathway (the chain of events) that causes this damage, researchers can now design targeted treatments that stop the problem at its source rather than just treating the symptoms

This study combines both animal models and human cell experiments, which strengthens the findings. The researchers tested multiple ways to block the harmful process, and all methods showed similar protective effects. However, the study was published in early 2026 and represents preliminary research. Animal studies don’t always translate directly to humans, so these findings need to be confirmed in human clinical trials before becoming standard medical treatments

What the Results Show

When researchers created areas of slow blood flow in mice arteries, the protective cells lining those arteries underwent ferroptosis (a special type of cell death involving iron and harmful molecules). This cell death led to more plaque buildup and atherosclerosis development. The researchers identified that a protein called P53 acts as the master switch that triggers this harmful process by turning off a protective mechanism called xCT.

When researchers blocked ferroptosis using the drug Fer-1, or boosted the protective protein GPX4, the mice developed significantly less artery plaque. Similarly, when they removed P53 or blocked it with inhibitors, the artery damage was prevented. These results were consistent across multiple experiments, suggesting the pathway is a reliable target for treatment.

The mechanism works like this: slow blood flow activates P53, which then shuts down xCT (a protective system that prevents harmful iron buildup). Without xCT working properly, iron accumulates inside cells and creates dangerous reactive oxygen species (harmful molecules), triggering ferroptosis and damaging the artery lining.

The study showed that the P53/xCT pathway is specifically important in endothelial cells (the artery lining cells), not in other cell types. This specificity is important because it suggests treatments targeting this pathway might avoid unwanted side effects in other tissues. The researchers also demonstrated that the process works the same way in both mouse models and human blood vessel cells grown in the lab, suggesting the findings may be relevant to human heart disease

This research builds on previous discoveries that ferroptosis (cell death from iron and harmful molecules) plays a role in heart disease. However, this is the first study to clearly show that slow blood flow specifically triggers ferroptosis through the P53 protein in artery-lining cells. Previous research had identified P53’s role in other types of cell death, but this study reveals a new and important function in preventing heart disease. The findings also explain why heart disease develops in specific locations (curved and branching arteries) where blood flow naturally slows down

This study was conducted in mice and laboratory cells, not in humans. Mice models of heart disease don’t perfectly replicate how the disease develops in people. The study didn’t test whether existing heart disease patients would benefit from blocking this pathway. The researchers also didn’t test long-term effects or potential side effects of blocking P53 or ferroptosis in living organisms over extended periods. Additionally, the sample size and specific numbers of animals used weren’t detailed in the abstract

The Bottom Line

Based on this research (moderate confidence level), future treatments that block the P53/xCT pathway or ferroptosis in artery-lining cells may help prevent heart disease. However, these are still experimental approaches. Current heart disease prevention remains most effective through proven methods: maintaining a healthy diet, regular exercise, not smoking, managing stress, and taking prescribed medications if recommended by your doctor. This research suggests new drug targets but doesn’t change current medical advice

This research is most relevant to people at high risk for heart disease, including those with family history of early heart attacks, high cholesterol, high blood pressure, or diabetes. It’s also important for researchers and pharmaceutical companies developing new heart disease treatments. People with existing heart disease should continue following their doctor’s current treatment plans while waiting for new therapies to be developed and tested in humans

If this research leads to human treatments, it will likely take 5-10 years before new drugs based on these findings reach patients. First, researchers must test safety and effectiveness in human clinical trials. Even then, new treatments would likely be used alongside current heart disease prevention strategies, not as replacements

Want to Apply This Research?

  • Track weekly heart health metrics including blood pressure readings, exercise minutes, and dietary fat intake. Users can monitor trends over time to see how lifestyle changes affect their cardiovascular risk factors
  • Set daily reminders for heart-healthy activities: 30 minutes of moderate exercise, eating one extra serving of vegetables, and checking blood pressure weekly. Users can log completion and see their consistency over time
  • Create a monthly heart health dashboard showing trends in blood pressure, exercise frequency, diet quality, and stress levels. Users can identify which lifestyle factors correlate with better or worse readings, helping them make informed adjustments

This research describes laboratory and animal studies that have not yet been tested in humans. The findings are preliminary and should not be used to change your current heart disease treatment or prevention plan. Always consult with your doctor before making changes to your diet, exercise routine, or medications. If you have risk factors for heart disease or existing heart disease, work with your healthcare provider to develop a personalized prevention and treatment plan based on proven, established therapies.