Cataract pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] , Associate Editor-In-Chief: Joseph Nasr, M.D.[2]
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Pathophysiology
The crystalline lens is an avascular structure composed of elongated fiber cells that are densely packed with specialized proteins known as crystallins, whose precise spatial organization and hydration are essential for maintaining lens transparency. The cytoskeleton of lens fiber cells contributes to their characteristic shape, while membrane protein channels regulate ionic and osmotic balance across the lens, supporting normal optical function.[1]
Lens transparency is preserved in part by protection of protein-bound sulfhydryl groups against oxidation through high intracellular concentrations of reduced glutathione. Crystallins exhibit long-term structural stability and are capable of absorbing short-wavelength visible light, ultraviolet radiation, and infrared radiation while maintaining transparency, thereby providing a protective role for enzymatic activity within the lens.[1]
With aging, progressive oxidative stress leads to an imbalance between the generation of reactive oxygen species and the lens’s ability to detoxify reactive intermediates or repair oxidative damage. Disruption of cellular redox homeostasis results in oxidative injury to proteins, lipids, and nucleic acids within lens cells.[1]
Age-related oxidative processes promote protein modification, aggregation, and insolubilization, resulting in increased light scattering and loss of lens transparency. Accumulation of damaged and aggregated crystallins contributes to breakdown of fiber cell membranes and progressive opacification of the lens.[1]
Aging also reduces the metabolic efficiency of the lens, increasing susceptibility to environmental and metabolic stressors. Alterations in glucose metabolism, impaired protein synthesis and transport, and declining membrane repair capacity further predispose the lens to cataract formation.[1]
Because mature lens fiber cells are denucleated and lack the ability to replace damaged components, maintenance of metabolic homeostasis depends on the lens epithelium and a limited population of metabolically active fiber cells. Progressive failure of this system results in steep metabolic gradients within the lens and contributes to localized opacities, including wedge-shaped or sectoral cataracts.[1]
Lens epithelial cells are continuously exposed to light and radiation stress, which may induce genetic and cellular damage. As defective cells cannot be extruded, they may undergo degradation or migrate toward the posterior capsule, where they contribute to the development of posterior subcapsular cataracts.[1]