Can Nazlı, Alaçamlı Göksu, Karalezli Aylin, Başsimitci Nermin
Department of Obstetrics and Gynecology, Faculty of Medicine, Mugla Sıtkı Koçman University, Turkey.
Department of Ophthalmology, Faculty of Medicine, Mugla University, Turkey.
J Int Med Res. 2025 Sep;53(9):3000605241306612. doi: 10.1177/03000605241306612. Epub 2025 Sep 9.
ObjectivePseudoexfoliation syndrome is a systemic disease of unknown etiology, seen in advanced ages, characterized by extracellular material accumulation in ocular tissues and visceral organs. Autophagy, which is a basic metabolic pathway, provides macromolecule recycling of the cell and maintains cell homeostasis by adapting to the cell's stress environment. The aim of this study was to examine the relationship between specific mechanisms of autophagy and pseudoexfoliation syndrome.MethodsIn this prospective-controlled study, anterior capsulorhexis materials obtained during cataract surgery were immunohistochemically compared between eyes with and without pseudoexfoliation syndrome using Image Tool Software for possible changes in autophagy, in terms of expression levels of Beclin 1, ATG5, ATG6, ATG12, p62, and LC3A/B autophagy markers.ResultsSignificant differences were observed between the anterior capsulorhexis materials of eyes with and without pseudoexfoliation syndrome, in terms of expression levels of some specific autophagy markers.ConclusionOur study may gain importance as it is the first study in which Beclin 1, ATG5, ATG6, ATG12, p62, and LC3A/B autophagy markers are examined prospectively in the etiopathogenesis of pseudoexfoliation syndrome, comprehensively and with a control group.
目的
假性剥脱综合征是一种病因不明的全身性疾病,多见于老年人,其特征是眼组织和内脏器官中细胞外物质的积累。自噬作为一种基本的代谢途径,可实现细胞内大分子的循环利用,并通过适应细胞的应激环境维持细胞内稳态。本研究旨在探讨自噬的特定机制与假性剥脱综合征之间的关系。
方法
在这项前瞻性对照研究中,使用Image Tool软件对白内障手术中获取的撕囊前囊膜材料进行免疫组织化学分析,比较有和没有假性剥脱综合征的眼睛之间自噬的可能变化,具体涉及Beclin 1、ATG5、ATG6、ATG12、p62和LC3A/B自噬标志物的表达水平。
结果
在有和没有假性剥脱综合征的眼睛的撕囊前囊膜材料中,某些特定自噬标志物的表达水平存在显著差异。
结论
我们的研究可能具有重要意义,因为这是第一项在前瞻性研究中,在假性剥脱综合征的发病机制中全面且有对照组地检测Beclin 1、ATG5、ATG6、ATG12、p62和LC3A/B自噬标志物的研究。