Scientists discovered that blocking a protein called SRC might help prevent blood vessels from aging too quickly. Using mice and lab-grown cells, researchers found that when they turned off SRC, the cells’ energy factories (mitochondria) worked better and cleaned up their waste more efficiently. This process, called mitophagy, is like taking out the trash in your cells. When SRC was blocked with a drug called KX2-391, mice on unhealthy diets showed less buildup in their arteries and healthier blood vessel walls. This discovery could lead to new treatments for heart disease and aging-related blood vessel problems.

The Quick Take

  • What they studied: Whether turning off a protein called SRC could slow down aging in blood vessels and improve how cells clean up damaged parts of themselves
  • Who participated: Mice genetically modified to develop heart disease, fed high-fat diets and given a diabetes-inducing chemical; also mouse blood vessel cells grown in laboratory dishes
  • Key finding: Blocking SRC with a drug reduced signs of aging in blood vessels, improved mitochondrial health, and reduced plaque buildup in arteries by activating a cellular cleanup process called mitophagy
  • What it means for you: This research suggests that future drugs targeting SRC might help prevent or slow blood vessel aging and heart disease, though human studies are still needed to confirm these benefits

The Research Details

Researchers used two main approaches to study vascular aging. First, they created mice that naturally develop heart disease (ApoE-/- mice) and fed them high-fat diets while injecting them with a chemical to cause diabetes-like conditions. This mimicked how blood vessels age in humans with unhealthy lifestyles. Second, they grew mouse blood vessel cells in dishes and exposed them to a cancer drug (doxorubicin) to make the cells age rapidly in a controlled way.

The team measured SRC protein levels in both models and found they were elevated. They then used a drug called KX2-391 to block SRC activity and observed what happened to the cells and blood vessels. They also used genetic techniques to remove SRC or a related protein called FUNDC1 to understand which proteins were responsible for the benefits.

This combination of animal and cell-based studies allowed researchers to see both how the treatment worked in a living system and what was happening at the cellular level.

Using both living animals and isolated cells is important because it shows whether a treatment works in a complex biological system (the whole body) and helps explain the exact mechanism at the cellular level. This approach strengthens confidence in the findings and helps researchers understand how to develop better treatments.

The study used established models of vascular aging recognized in the scientific community. The researchers confirmed their findings using multiple methods (blocking the protein with drugs, removing it genetically, and overproducing it). However, the study was conducted only in mice and cells, not humans, so results may not directly translate to people. The specific sample sizes for animal groups were not provided in the abstract, which limits assessment of statistical power.

What the Results Show

When researchers blocked SRC using the drug KX2-391, several positive changes occurred. In mice with accelerated vascular aging, the drug reduced plaque buildup in arteries and made the protective fibrous cap surrounding plaques more stable—both important for preventing heart attacks.

At the cellular level, blocking SRC improved the appearance and function of mitochondria (the energy-producing parts of cells). More importantly, it activated a cleanup process called mitophagy, where cells remove damaged mitochondria. This cellular housekeeping is crucial because damaged mitochondria contribute to aging.

When researchers removed the SRC gene from aging cells, the cells showed reduced signs of senescence (aging). Conversely, when they added extra SRC, cells aged faster and the protective effects of the drug disappeared. This confirmed that SRC directly causes the aging process in blood vessel cells.

The research identified FUNDC1 as the key protein through which SRC works. When FUNDC1 was removed, the anti-aging benefits of blocking SRC disappeared entirely, proving this protein is essential for the treatment’s effects.

The study found that SRC works by attaching a phosphate group to FUNDC1 at a specific location (Tyr18). When SRC was blocked, this phosphorylation decreased, which allowed mitophagy to work better. This molecular detail explains the mechanism of action and suggests why the treatment is effective.

Previous research had linked SRC to aging in general, but its specific role in blood vessel aging was unknown. This study fills that gap by showing SRC is a key regulator of mitochondrial health in blood vessels. The findings align with growing evidence that mitochondrial dysfunction and impaired cellular cleanup are central to vascular aging and atherosclerosis development.

This research was conducted entirely in mice and laboratory cells, not in humans, so results may not directly apply to people. The study did not test the drug KX2-391 in humans or assess its safety and effectiveness in clinical settings. Additionally, the abstract does not specify how many animals were used in each group, making it difficult to evaluate the statistical reliability of the findings. Long-term effects of SRC inhibition were not examined, so it’s unclear whether benefits persist over time or if side effects might develop.

The Bottom Line

Based on this research, SRC inhibition appears promising for preventing vascular aging and atherosclerosis (moderate confidence level). However, these findings are preliminary and based on animal studies. Do not change your current medical treatments based on this research alone. If you have heart disease or cardiovascular risk factors, continue following your doctor’s recommendations regarding diet, exercise, and medications.

This research is most relevant to people at risk for heart disease, those with high cholesterol or diabetes, and individuals interested in aging-related health conditions. It may eventually benefit people with atherosclerosis, but currently, it’s primarily of interest to researchers and pharmaceutical companies developing new treatments. This is not yet a treatment available to patients.

If SRC-inhibiting drugs are developed and tested in humans, it would likely take 5-10 years before they become available as treatments. Benefits would probably develop gradually over weeks to months of treatment, similar to other cardiovascular medications.

Want to Apply This Research?

  • Track cardiovascular health markers: record blood pressure readings weekly, monitor resting heart rate daily, and log any symptoms like chest discomfort or shortness of breath to share with your healthcare provider
  • Implement lifestyle changes that support vascular health while waiting for potential new treatments: adopt a heart-healthy diet low in saturated fats, exercise for 150 minutes weekly, maintain a healthy weight, and manage stress through meditation or yoga
  • Set monthly reminders to review your cardiovascular health metrics and schedule annual check-ups with your doctor to assess blood pressure, cholesterol levels, and overall vascular function through standard medical tests

This research is preliminary and based on animal studies and laboratory cells, not human trials. SRC-inhibiting drugs are not currently available as treatments for vascular aging or heart disease. Do not discontinue or change any prescribed cardiovascular medications based on this information. If you have concerns about vascular health or aging, consult with your healthcare provider about evidence-based treatments and lifestyle modifications. This summary is for educational purposes only and should not be considered medical advice.