Researchers from Johns Hopkins University School of Medicine discovered that tobacco smoke hastens the aging process in eye cells by inducing epigenetic modifications—alterations in gene function without changing the underlying DNA sequence. These findings have been detailed in Proceedings of the National Academy of Sciences (PNAS).
It is a known fact that smokers face an approximately fourfold heightened risk of age-related macular degeneration (AMD), a primary cause of vision loss in individuals past the age of 50. Yet, the biological pathways linking smoking to AMD remained poorly understood until now.
For this novel study, scientists investigated the response of retinal pigment epithelium (RPE) cells—which sustain light-sensing photoreceptors—to both short-term and prolonged exposure to cigarette smoke.
Tests conducted on both young and aged mice demonstrated that smoke exposure dampens the activity of genes essential for healthy retinal cell operation. Furthermore, it reduced the accessibility of chromatin, the complex structure governing gene activation and repression. Consequently, these cells exhibited diminished stress resilience and displayed accelerated aging markers mirroring the changes seen in human macular degeneration.
Crucially, the biological response varied based on the subject’s age. In younger subjects, defensive mechanisms became engaged, boosting the expression of genes linked to inflammation control, mitochondrial performance, and cellular “housekeeping” processes. In contrast, elderly test subjects showed almost no such compensatory response, resulting in significantly higher frequencies of cell damage and death.
Further tests using human tissues validated the similarity of these observed molecular changes, suggesting that these research outcomes may be relevant to the human population. Moving forward, the research team intends to determine which of these epigenetic shifts are reversible and which contribute to permanent vision deterioration.
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