Oxidative stress, epigenetic regulation and pathological processes of lens epithelial cells underlying diabetic cataract
- AOPR Vol. 3, Issue 4, Pages: 180-186(2023)
- 作者机构：
1. Shaanxi Eye Hospital, Xi'an People's Hospital (Xi'an Fourth Hospital), Affiliated People's Hospital of Northwest University,Shaanxi,Xi'an,China
2. Xi'an Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Medical Research, Northwestern Polytechnical University,Shaanxi,Xi'an,China
- 作者简介：
- 基金信息：
DOI：10.1016/j.aopr.2023.10.001
CLC：
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Oxidative stress, epigenetic regulation and pathological processes of lens epithelial cells underlying diabetic cataract. [J]. AOPR 3(4):180-186(2023)
Oxidative stress, epigenetic regulation and pathological processes of lens epithelial cells underlying diabetic cataract. [J]. AOPR 3(4):180-186(2023) DOI： 10.1016/j.aopr.2023.10.001.
摘要
Background,Cataract is a blinding disease worldwide. It is an age-related disease that mainly occurs in people over 65 years old. Cataract is also prevalent in patients with diabetes mellites (DM). The pathological mechanisms underlying diabetic cataract (DC) are more complex than that of age-related cataract. Studies have identified that polyol pathway, advanced glycation end products (AGEs) and oxidative stress are the primary pathogenesis of DC. In recent years, molecular-level regulations and pathological processes of lens epithelial cells (LECs) have been confirmed to play roles in the initiation and progression of DC. A comprehensive understanding and elucidation of how chronic hyperglycemia drives molecular-level regulations and cytopathological processes in the lens will shed lights on the prevention, delay and treatment of DC.,Main text,Excessive glucose in the lens enhances polyol pathway and AGEs formation. Polyol pathway causes imbalance in the ratio of NADPH/NADP,+, and NADH/NAD,+,. Decrease in NADPH/NADP,+, ratio compromises antioxidant enzymes, while increase in NADH/NAD,+, ratio promotes reactive oxygen species (ROS) overproduction in mitochondria, resulting in oxidative stress. Oxidative stress in the lens causes oxidation of DNA, proteins and lipids, leading to abnormalities in their structure and functions. Glycation of proteins by AGEs decreases solubility of proteins. High glucose triggered epigenetic regulations directly or indirectly affect expressions of genes and proteins in LECs. Changes in autophagic activity, increases in fibrosis and apoptosis of LECs destroy the morphological structure and physiological functions of the lens epithelium, disrupting lens homeostasis.,Conclusions,In both diabetic animal models and diabetics, oxidative stress plays crucial roles in the formation of cataract. Epigenetic regulations, include lncRNA, circRNA, microRNA, methylation of RNA and DNA, histone acetylation and pathological processes, include autophagy, fibrosis and apoptosis of LECs also involved in DC.
Abstract
Background,Cataract is a blinding disease worldwide. It is an age-related disease that mainly occurs in people over 65 years old. Cataract is also prevalent in patients with diabetes mellites (DM). The pathological mechanisms underlying diabetic cataract (DC) are more complex than that of age-related cataract. Studies have identified that polyol pathway, advanced glycation end products (AGEs) and oxidative stress are the primary pathogenesis of DC. In recent years, molecular-level regulations and pathological processes of lens epithelial cells (LECs) have been confirmed to play roles in the initiation and progression of DC. A comprehensive understanding and elucidation of how chronic hyperglycemia drives molecular-level regulations and cytopathological processes in the lens will shed lights on the prevention, delay and treatment of DC.,Main text,Excessive glucose in the lens enhances polyol pathway and AGEs formation. Polyol pathway causes imbalance in the ratio of NADPH/NADP,+, and NADH/NAD,+,. Decrease in NADPH/NADP,+, ratio compromises antioxidant enzymes, while increase in NADH/NAD,+, ratio promotes reactive oxygen species (ROS) overproduction in mitochondria, resulting in oxidative stress. Oxidative stress in the lens causes oxidation of DNA, proteins and lipids, leading to abnormalities in their structure and functions. Glycation of proteins by AGEs decreases solubility of proteins. High glucose triggered epigenetic regulations directly or indirectly affect expressions of genes and proteins in LECs. Changes in autophagic activity, increases in fibrosis and apoptosis of LECs destroy the morphological structure and physiological functions of the lens epithelium, disrupting lens homeostasis.,Conclusions,In both diabetic animal models and diabetics, oxidative stress plays crucial roles in the formation of cataract. Epigenetic regulations, include lncRNA, circRNA, microRNA, methylation of RNA and DNA, histone acetylation and pathological processes, include autophagy, fibrosis and apoptosis of LECs also involved in DC.
关键词
Oxidative stressEpigenetic regulationAutophagyFibrosisApoptosisDiabetic cataract
Keywords
Oxidative stressEpigenetic regulationAutophagyFibrosisApoptosisDiabetic cataract
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