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How hyperglycemia promotes ocular diseases: An overview of molecular mechanisms
Shuwei Li1, Siyang Liu1, Xingtao Zhou1
1Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China; Key Laboratory of Myopia and Related Eye Diseases, NHC, Key Laboratory of Myopia and Related Eye Diseases, Chinese Academy of Medical Sciences, Shanghai, 200031, China; Shanghai Research Center of Ophthalmology and Optometry, Shanghai, 200031, China; Shanghai Engineering Research Center of Laser and Autostereoscopic 3D for Vision Care, Shanghai, 200031, China.
Abstract:
Ocular diseases result from a complex interaction of environmental and metabolic factors. The increasingly prevalent sedentary lifestyle and dietary patterns characterized by high sugar and ultra-processed food intake substantially elevate the risk of hyperglycemia. Hyperglycemia induces dysregulation of core metabolic pathways, such as overactivation of the polyol and hexosamine pathways, aberrant activation of protein kinase C, and accumulation of advanced glycation end products. Hyperglycemia further triggers tissue-specific molecular and cellular events in various ocular structures. These mechanisms collectively contribute to ocular damage and drive the progression of sight-threatening ocular diseases, including myopia, glaucoma, diabetic retinopathy, diabetic cataract, and diabetic keratopathy. A comprehensive understanding of these mechanisms provides a critical theoretical foundation for developing precision strategies for the prevention and management of hyperglycemia-associated ocular complications.
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