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Spermidine: An Autophagy-Inducing Polyamine for Eye HealthSpermidine is a naturally occurring polyamine found in all cells and in many aging-friendly foods. It has recently attracted attention as an autophagy inducer and “longevity” nutrient. Autophagy is a cellular “cleanup” process that degrades damaged proteins and organelles (including mitochondria) to maintain cell health. In model organisms, spermidine robustly extends lifespan, likely by reactivating autophagy () (). In cultured cells and animals, spermidine suppresses the histone acetyltransferase EP300, lowering protein acetylation and thereby accelerating autophagic flux (). At the same time, spermidine has a large safety margin; to date “no adverse effects of exogenous supply of spermidine have been reported” (), and dosing studies in humans (~1–3 mg/day) have increased intake by only ~10–20% over diet without toxicity (). Autophagy and Mitochondrial Quality ControlBy inducing autophagy, spermidine helps cells clear damaged components and maintain mitochondrial health. For example, chronic spermidine feeding in aged mice enhanced cardiac autophagy and mitophagy, improved mitochondrial respiration, and reduced markers of cellular aging (). These cardioprotective effects required intact autophagy machinery: mice lacking the autophagy gene Atg5 in heart cells did not benefit from spermidine (). Improved mitochondrial quality is also seen in neurons: spermidine restored bioenergetics in aged human neurons and in animal models by boosting mitochondrial respiration and ATP production (). Such mitophagy-promoting effects are relevant to long-lived neurons (like retinal ganglion cells) that depend on mitochondrial fitness. Retinal Ganglion Cell Survival and Neuroprotection Evidence is emerging that spermidine can protect retinal neurons. In a mouse optic nerve injury model (simulating neurodegeneration), daily oral spermidine dramatically reduced retinal ganglion cell (RGC) death and preserved retinal structure (). The study found that spermidine acts as a free-radical scavenger in this context: it inhibited retinal oxidative stress signaling (ASK1–p38 kinase pathway) and lowered expression of inflammatory mediators such as iNOS in microglia () (). Spermidine-treated mice also showed less microglial accumulation in the retina and enhanced optic nerve regeneration (). In other words, spermidine not only prevented RGC apoptosis but even improved nerve regrowth after injury. These findings led the authors to conclude that “spermidine stimulates neuroprotection as well as neuroregeneration” (), suggesting potential benefit for diseases like glaucoma.In a genetic mouse model of normal-tension glaucoma (EAAC1 knockout), spermidine in the drinking water also protected vision even though intraocular pressure was unchanged. Mice receiving 30 mM spermidine showed less retinal thinning and better visual function than untreated controls (). This protection was linked to antioxidant effects: spermidine reduced lipid-peroxidation (4-HNE) levels in the retina, indicating it counteracts oxidative stress (). Thus, while spermidine does not lower IOP directly, it seems to boost optic nerve resilience by quenching reactive oxygen species and inflammation. In summary, in multiple retinal models spermidine has acted as an endogenous antioxidant/autophagy booster to preserve RGCs and visual function () ().Spermidine, Longevity and Cardiovascular HealthPopulation studies support spermidine’s role in longevity and cardio