A new preclinical study suggests that a high-sodium diet may do more than raise blood pressure; it could also accelerate aging in the immune system and blood vessels by triggering inflammatory processes that damage vascular function.

Researchers at the University of South Alabama found that mice fed a high-salt diet developed rapid impairment in small artery function within four weeks, reducing the blood vessels’ ability to relax and regulate blood flow effectively.

The findings, published in the Journal of the American Heart Association, indicate that the damage was not caused by direct salt exposure to blood vessel cells. Instead, the study suggests the body’s immune response may play a central role.

According to the researchers, high sodium intake may stimulate the release of a signaling molecule called interleukin-16 (IL-16), which appears to push vascular cells into a state known as cellular senescence. In this state, cells stop dividing and begin releasing inflammatory compounds that can harm surrounding tissue.

The study also found that senescent cells failed to produce nitric oxide, a key molecule that allows blood vessels to remain flexible and expand properly in response to blood flow demands.

To test whether the damage could be reversed, researchers used a senolytic compound called navitoclax, a drug originally developed for cancer treatment that targets and removes aged or dysfunctional cells. In the mouse models, treatment restored much of the blood vessels’ normal function.

However, the researchers cautioned that the findings remain preliminary. They noted that results in animal studies do not always translate directly to humans, and the safety profile of senolytic drugs is still under investigation.

The team also said it has not yet confirmed whether the IL-16 pathway plays the same role in human vascular aging, and previous studies of similar drugs have produced mixed results.

While the research adds to growing evidence linking diet and cardiovascular health, the authors emphasized that further human studies are needed before any clinical conclusions can be drawn.