Abstract
Cataracts in diabetes mellitus lead to decreased visual function and blindness. Cataract surgery for diabetes mellitus has limitations and complications. The search for effective means of conservative cataract therapy continues. The review presents the analysis of data from scientific sources, mainly for 2015–2020 using Internet resources (PubMed, Web of Science, Medline, eLibrary.Ru, Cyberleninka). In the work, diabetic cataractogenesis is presented as a sum of interrelated pathobiochemical processes. The main ones are the polyol pathway of glucose conversion, non-enzymatic glycation and oxidative modification of lens proteins, which are enhanced in diabetes mellitus. The lens has a high protein content. The formation of high molecular weight protein aggregates is of particular importance for the appearance of light scattering zones and a decrease in lens transparency. This review presents data on anti-cataract compounds that affect post-translational crystallin modification, prevent osmotic and oxidative stress in the lens, and exhibit antiglycation properties. This information shows that the search for means of pharmacological correction of cataractogenesis should be carried out among compounds with antioxidant and antiglycation activity.
Highlights
ДИАБЕТИЧЕСКИЙ КАТАРАКТОГЕНЕЗ Катаракта является одной из основных причин снижения остроты и качества зрения у пациентов с сахарным диабетом (СД) [1]
Роль АР в диабетическом катарактогенезе подтверждается работой, в которой было показано, что хрусталики крыс, имеющие низкую экспрессию АР или не имеющие её вовсе, при инкубировании в среде с глюкозой устойчивы к развитию диабетической катаракты [9]
Prevention of α-crystallin glycation and aggregation using l-lysine results in the inhibition of in vitro catalase heat-induced-aggregation and suppression of cataract formation in the diabetic rat
Summary
ДИАБЕТИЧЕСКИЙ КАТАРАКТОГЕНЕЗ Катаракта является одной из основных причин снижения остроты и качества зрения у пациентов с сахарным диабетом (СД) [1]. Гликирование α-кристаллина различными гликирующими агентами, включая глюкозу и МГ, приводит к снижению его шапероноподобной активности, а также к накоплению карбонильных белковых групп и КПГ в хрусталиках, главным образом, КМЛ [20].
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