New preclinical research suggests a high-salt diet may trigger immune signals that prematurely age blood vessels, adding a possible mechanism to sodium’s heart risks.
A high-salt diet may do more than raise blood pressure: New preclinical research suggests excess sodium can prompt the immune system to send signals that prematurely age blood vessels.
The study, recently published in the Journal of the American Heart Association, examined mice fed a high-salt diet and found a rapid decline in the function of small arteries that help regulate blood flow. After four weeks of high sodium intake, those vessels lost much of their ability to relax, according to a press release cited in the report.
The findings add a possible biological explanation to the long-established link between excess salt and cardiovascular risk. But the work remains early-stage: It was conducted in mice, and researchers have not confirmed whether the same process is a main driver of vascular aging in people.
Scientists at the University of South Alabama found that cells lining the mice’s blood vessels had entered cellular senescence, a state often described as premature cellular aging. In that state, cells stop dividing and can release inflammatory signals that may harm nearby tissue.
When researchers exposed blood vessel cells directly to salt in a lab dish, however, the cells did not show the same harmful effects. That result suggested the damage was not caused by salt acting directly on the vessel lining, but by another process in the body.
The researchers identified a possible culprit: interleukin-16, or IL-16, an immune-system messenger molecule. The study suggests excess salt may trigger immune cells to release IL-16, which then appears to push blood vessel cells toward premature aging.
Once those cells age, they produce less nitric oxide, a gas that helps arteries dilate and remain flexible. Reduced nitric oxide can make vessels less responsive to the body’s changing blood-flow needs.
The team also tested whether the damage could be reversed. Using navitoclax, a cancer drug in a class of experimental treatments known as senolytics, researchers were able to clear out aged and dysfunctional cells in salt-fed mice and restore near-normal blood vessel function, according to the report.
That finding does not mean the drug is ready to treat diet-related vascular aging. The researchers cautioned that translating results from animal models to human treatment remains a major hurdle. Senolytic drugs such as navitoclax are still being studied for safety, and previous trials have shown mixed findings on their effects on artery plaque.
For now, the study points to a potential immune pathway linking high sodium intake to vascular decline — and to the need for further research to determine whether the same mechanism is active in humans.
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