Recent insights into the pathomechanisms of cataract development in diabetic patients

Diabetes mellitus (DM), a prevalent metabolic disorder characterized by chronic hyperglycemia, disrupts systemic homeostasis and affects multiple tissues, including the eye lens, where cataract is a common diabetic complication. Crystallin proteins constitute the majority of the proteins in the eye lens. One of their characteristics is a long lifespan, which makes them susceptible to the accumulation of physical and chemical damage, particularly in the context of diabetes. Therefore, protecting these proteins is crucial to maintaining eye lens transparency. In diabetes, crystallin proteins sustain various forms of damage that can significantly alter their structures and functions, ultimately leading to cataract development. Many studies have been conducted to uncover the molecular mechanisms behind the development of diabetic cataracts. Well-established contributors to diabetic cataract include oxidative stress, protein glycation and glycoxidation, enhanced photodamage to lens proteins, and dysregulated concentrations of specific elements. This review article aims to provide an up-to-date overview of the processes involved in the development of cataracts in diabetic patients.