The study identifies Clostridium sp. ASF356 as a key bacterium that converts phenylalanine into phenylacetic acid (PAA), impacting both mice and humans.

PAA, a byproduct of phenylalanine breakdown, accumulates with age and contributes to endothelial cell senescence, halting their division.

The research established a causal relationship between PAA exposure and increased senescence markers in endothelial cells, leading to dysfunction.

In aged mice, an increased abundance of microbial genes related to the conversion of phenylalanine to PAA was noted, correlating with elevated plasma PAA levels.

Using antibiotics to eliminate these bacteria in mice resulted in reduced PAA levels, confirming their role in its accumulation.

Recent research published in Nature Aging highlights the significant role of gut bacteria in influencing blood vessel aging.

Endothelial dysfunction, which occurs with aging, is a significant contributor to cardiovascular diseases, the leading cause of death globally.

This dysfunction triggers inflammation and stiffens blood vessels, further increasing the risk of cardiovascular issues.

Analysis of health data from the TwinsUK cohort revealed age-associated increases in PAA and its correlation with endothelial dysfunction.

Sodium acetate, an anti-inflammatory short-chain fatty acid, was shown to mitigate the effects of PAA on endothelial cells, promoting healthier function.

Adding sodium acetate to aged endothelial cells restored some function, suggesting potential therapeutic avenues for improving vascular health.

Further research is needed to explore medications aimed at lowering PAA levels to enhance vascular health and combat aging.