An unexpected factor in accelerated eye aging has been identified

Scientists from the Johns Hopkins University School of Medicine have discovered that cigarette smoke accelerates the aging of eye cells through epigenetic changes — disruptions in gene function without alterations to the DNA itself. The results of the study have been published in the journal Proceedings of the National Academy of Sciences (PNAS).

It is known that smokers are approximately four times more likely to develop age-related macular degeneration — one of the leading causes of vision loss after the age of 50. However, the biological mechanisms behind this link have long remained unclear.

In the new study, scientists examined how retinal pigment epithelium (RPE) cells, which support the function of light-sensitive photoreceptors, respond to short-term and prolonged exposure to cigarette smoke.

Experiments on young and aged mice showed that smoke suppresses the activity of genes essential for the normal functioning of retinal cells and also reduces chromatin accessibility — the structure that regulates the turning on and off of genes. As a result, the cells coped with stress less effectively and exhibited signs of accelerated aging resembling the changes seen in human macular degeneration.

The body's response also depended on age. In young animals, protective mechanisms were activated — there was increased activity of genes associated with inflammation control, mitochondrial function, and cellular "self-cleaning" processes. In aged mice, this compensatory response was nearly absent, causing cells to become damaged and die significantly more often.

Additional experiments with human tissues confirmed the similarity of the identified molecular changes, suggesting the potential applicability of the results to humans. Going forward, the researchers plan to determine which epigenetic changes can be reversed and which lead to irreversible vision deterioration.