The key mechanisms and intervention strategies of cell-type-specific mitochondrial metabolism in ophthalmic diseases

Abstract

The eye is one of the most metabolically active organs, and mitochondria serve as the central hub for cellular energy metabolism by providing adenosine triphosphate through oxidative phosphorylation. Disruption of mitochondrial metabolism—including insufficient adenosine triphosphate synthesis, excessive production of reactive oxygen species, and dysregulated quality control—can trigger various ocular diseases. Common blinding diseases such as myopia, diabetic retinopathy, and glaucoma are closely associated with mitochondrial dysfunction in specific cell types. This review delineates the mechanisms by which metabolic adaptations in scleral fibroblasts induce myopia and the synergistic action of lipofuscin, the high-glucose-triggered mitochondrial reactive oxygen species bursts and metabolic memory in diabetic retinopathy, and the roles of mitochondrial dynamics imbalance and energy exhaustion in trabecular meshwork cells in glaucoma. Based on these mechanisms, the article proposes intervention strategies targeting mitochondrial antioxidant defense, enhancing mitochondrial biogenesis, regulating mitochondrial dynamics, and restoring mitophagy, aiming for precise prevention and treatment of ocular diseases at the mitochondrial level.