Review on Lenticular Metabolism and Cataract

Cataract, characterized by the opacification of the eye lens, remains the leading cause of blindness globally. Among various etiological factors, disruptions in lenticular metabolism have been recognized as a critical contributor to cataractogenesis. The avascular nature of the lens necessitates a highly regulated metabolic environment to maintain its transparency and function. This review explores the intricate metabolic pathways within the lens, particularly focusing on glucose metabolism through glycolysis, the pentose phosphate pathway, and the sorbitol (polyol) pathway. Under physiological conditions, these pathways support cellular homeostasis, maintain redox balance, and provide essential metabolic substrates. However, metabolic imbalances-particularly those associated with diabetes mellitus-can lead to excessive accumulation of sorbitol and oxidative stress, thereby inducing osmotic imbalance, protein aggregation, and ultimately, lens opacification. Furthermore, the review highlights the role of antioxidant defenses, including glutathione and enzymatic systems like superoxide dismutase and catalase, which are vital in protecting the lens from oxidative damage. Age-related decline in these defenses, along with cumulative metabolic insults, contributes significantly to cataract formation. Genetic factors influencing enzyme activities and transporter functions are also examined for their role in individual susceptibility to metabolic cataracts. Understanding the biochemical and molecular mechanisms of lenticular metabolism offers insights into potential therapeutic targets for delaying or preventing cataract development. This review underscores the importance of maintaining metabolic integrity and oxidative balance within the lens as a strategy for cataract prevention and management.