Cigarette Smoke Disrupts Eye Cell Mitochondria, Pointing to Macular Degeneration Risk

The work, published in Free Radical Biology & Medicine in 2026, is a cell and mouse study, not a human trial. The researchers exposed lab-grown human retinal pigment epithelium cells, known as ARPE-19 cells, and mice to cigarette smoke condensate, a concentrated extract of smoke.

Age-related macular degeneration, or AMD, is the leading cause of blindness in the elderly, according to the paper. It damages central vision. The retinal pigment epithelium, or RPE, is a layer of support cells behind the light-sensing cells of the retina. The authors suspected that smoking speeds AMD by pushing these cells into senescence, a state in which cells stop dividing and function poorly with age.

Low-dose smoke condensate did produce that picture. The cells showed more markers of senescence and signs of mitochondrial dysfunction. Mitochondria are the small structures that supply a cell with energy. Mice also showed impaired retinal function. In a separate experiment, mice exposed to cigarette smoke in a smoking chamber for six months showed RPE senescence features as well.

The mitochondria changed shape in two phases. Early on, they broke into fragments. Later, they fused into overly connected networks, a state called hyperfusion. At the same time, the cells were worse at mitophagy, the process of clearing damaged mitochondria. They also renewed their mitochondria less and made fewer new ones.

The team traced part of this to a protein called DRP1, which helps mitochondria divide. Smoke condensate raised phosphorylation of DRP1, a chemical tag that changes how the protein works. It also promoted cleavage, or cutting, of a mitochondrial enzyme called PGAM5. The study links this to reduced DRP1dependent division, more oxidative stress in mitochondria, and activation of mTOR, a signaling pathway tied to cell growth and ageing.

Genetic tests supported a causal role in the cells. Overexpressing a DRP1 mutant with reduced activity, called K38A, mimicked the senescence caused by smoke condensate. Overexpressing a phosphodeficient DRP1 mutant, called S637A, significantly reduced both mTOR signaling and smoke-induced senescence. It did so by restoring the balance of mitochondrial division, improving mitochondrial quality control and lowering oxidative stress.

There are clear limits. The work used cells and mice, and condensate is not the same as breathing smoke. The authors say the specific mechanisms still need validation in a chronic cigarette smoke model. Although they confirmed the senescence features in mice after six months of smoke, the detailed mitochondrial findings were not shown to hold there. Nothing here shows that any DRP1-targeting approach would help people. The authors say only that modulating RPE mitochondrial dynamics holds therapeutic potential for delaying AMD progression.

For you

For readers, the practical message is modest. The study adds a possible biological explanation for why smoking is linked to AMD, and it does not test any treatment or lifestyle change. What to watch next: whether the mitochondrial mechanisms are confirmed in chronic smoke models, and whether they appear in human eye tissue.

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