氧化应激,表观遗传调节和透镜上皮细胞的病理过程是糖尿病白内障的基础
Zaoxia Guo1, Xiaopan Ma1, Rui Xue Zhang2
1Shaanxi Eye Hospital, Xi'an People's Hospital (Xi'an Fourth Hospital), Affiliated People's Hospital of Northwest University, Xi'an, Shaanxi, China.
Advances in ophthalmology practice and research
|December 18, 2023
概括
糖尿病白内障 (DC) 涉及复杂的机制,如多途径,先进的糖化终产物 (AGEs) 和氧化应激. 了解透镜上皮细胞中的这些分子变化是预防和治疗这种视力损伤的关键.
科学领域:
- 眼科医生 眼科 眼科
- 内分泌学 在内分泌学.
- 细胞生物学 细胞生物学
背景情况:
- 糖尿病白内障 (DC) 是导致失明的重要原因,特别是在65岁以上和糖尿病患者中.
- DC的发病过程比与年龄相关的白内障更为复杂,涉及多途径,先进的糖化终产物 (AGEs) 和氧化应激.
- 镜片上皮细胞 (LECs) 经历由慢性高血糖症驱动的分子和细胞病理变化,有助于DC启动和进展.
研究的目的:
- 阐明糖尿病白内障中慢性高血糖症驱动的透镜中的分子机制和细胞病理过程.
- 为糖尿病白内障的预防,延迟和治疗策略提供见解.
主要方法:
- 在高葡萄糖条件下分析聚醇路径和先进糖化最终产品 (AGE) 的形成.
- 评估氧化应激标志物,包括活性氧物种 (ROS) 生产和抗氧化酶活性.
- 在透镜上皮细胞中研究表观遗传规则 (lncRNA,circRNA,microRNA,DNA/RNA甲基化,基因素乙化) 和细胞过程 (自,纤维化,亡).
主要成果:
- 过度的葡萄糖代谢通过多途径破坏细胞的氧化还原平衡 (NADPH/NADP+,NADH/NAD+),导致氧化应激.
- 氧化应激会对DNA,蛋白质和脂质造成损伤,改变透镜细胞的结构和功能.
- AGEs降低了蛋白质溶解度,而表观遗传变化和改变的细胞过程 (自,纤维化,亡) 破坏了透镜平衡,并导致白内障的形成.
结论:
- 氧化应激是糖尿病白内障形成的关键因素,在动物模型和人类糖尿病患者中都是如此.
- 在LEC中表观遗传修饰 (lncRNA,circRNA,microRNA,甲基化,基因素乙化) 和细胞病理 (自,纤维化,亡) 是DC发展的组成部分.
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