Coenzyme Q10 as a Mitochondrial Adjunct in Glaucoma and Lifespan Health

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Introduction Glaucoma is a progressive optic neuropathy marked by retinal ganglion cell (RGC) death and visual field loss (). Although lowering intraocular pressure (IOP) is the mainstay of treatment, many patients continue to lose vision despite controlled IOP, suggesting additional factors contribute to injury (). Mitochondrial dysfunction and oxidative stress are increasingly recognized in glaucomatous optic nerve damage (). Coenzyme Q10 (CoQ10) – a lipophilic cofactor of mitochondrial oxidative phosphorylation – emerges as a candidate neuroprotectant. CoQ10 shuttles electrons between complexes I/II and complex III in the electron transport chain and also scavenges reactive oxygen species (ROS) () (). In tissues with high energy demand and low antioxidant reserve, such as the retina and optic nerve, CoQ10 may support cellular bioenergetics and reduce oxidative damage. This article reviews CoQ10’s mitochondrial and antioxidant roles in the eye, evidence from animal and clinical glaucoma studies (including interactions with IOP-lowering drugs), and related systemic findings in aging and cardiometabolic health. We also discuss CoQ10 bioavailability, safety, and gaps in clinical evidence for glaucoma endpoints. CoQ10 in Mitochondrial Energy Metabolism CoQ10 is synthesized endogenously by mitochondria and is essential for adenosine triphosphate (ATP) production. In the inner mitochondrial membrane, ubiquinone (CoQ10) accepts electrons from complex I and II and transfers them to complex III, driving proton pumping and ATP synthesis via oxidative phosphorylation () (). Nearly every cell in the body contains CoQ10, with especially high concentrations in tissues with large mitochondria – such as the heart, brain, and retina () (). Studies indicate that CoQ10 levels decline with age or when biosynthesis is impaired; this decline may limit mitochondrial efficiency and increase oxidative stress (). In fact, aging, chronic disease and some medications (e.g. statins) can lower tissue CoQ10 levels, potentially contributing to cellular dysfunction (). Oral CoQ10 supplementation (300 mg/day or more) raises circulating and tissue CoQ10 and has shown benefits in disorders associated with mitochondrial dysfunction (). CoQ10 as an Antioxidant in the Retina and Optic Nerve Beyond its role in the electron transport chain, CoQ10 is a potent antioxidant. In its reduced form (ubiquinol), it directly neutralizes ROS and regenerates other antioxidants in membranes () (). The retina (particularly photoreceptors and RGCs) consumes oxygen at a very high rate and is susceptible to oxidative injury. CoQ10 is abundant in retinal mitochondria, and experimental studies show it can protect retinal cells from oxidative damage. For example, a seminal review noted that topical CoQ10 halted RGC apoptosis in rat glaucoma models (). Likewise, systemic CoQ10 in murine glaucoma preserved optic nerve axons by inhibiting oxidative-stress enzymes (lowering SOD2 and HO-1 expression) (). These findings support the concept that CoQ10 maintains oxidative phosphorylation while countering excessive ROS in retinal and optic nerve tissues. In vitro, CoQ10 has been shown to prevent glutamate excitotoxic injury to neurons – a mechanism relevant to glaucoma – which may reflect its mitochondrial support as well as its radical-scavenging activity () (). Importantly, CoQ10 can modulate glial responses: it inhibits stress-induced astrocyte activation in the optic nerve head and preserves ex