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角膜内皮细胞（CECs）是维持角膜透明性和稳态的关键功能细胞。白内障超声乳化术（PHACO）是目前治疗白内障的主流手术方式，但术中超声能量、机械刺激及灌注压力波动等因素可造成不同程度的角膜内皮损伤。糖尿病（DM）患者长期处于高糖微环境，可通过多元醇通路激活、晚期糖基化终产物/晚期糖基化终产物受体（AGEs/RAGE）轴介导的炎症反应、氧化应激、内质网应激及线粒体功能障碍等机制导致CECs屏障功能和泵功能受损。在DM所致基础损伤的背景下，PHACO相关损伤因素可进一步加重角膜内皮损害，二者相互叠加可能促进术后角膜水肿、CECs丢失、角膜失代偿及视功能恢复延迟等并发症的发生。明确DM患者PHACO相关角膜内皮损伤机制，并总结围手术期防护策略，有助于为DM患者PHACO围手术期角膜内皮保护及相关并发症防治提供参考。
Abstract：Corneal endothelial cells(CECs) are a crucial structure for maintaining corneal transparency and homeostasis.Phacoemulsification(PHACO) is currently the mainstream surgical approach for treating cataracts; however, factors such as intraoperative ultrasound energy, mechanical stimulation and fluctuations in perfusion pressure can cause varying degrees of corneal endothelial damage.Patients with diabetes mellitus(DM) are exposed to a chronic hyperglycaemic microenvironment, which can impair the barrier and pumping functions of CECs through mechanisms such as activation of the polyol pathway, inflammation mediated by the advanced glycation end-products(AGEs)/receptor for advanced glycation end-products(RAGE) axis, oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction.On top of the underlying damage caused by DM, PHACO-related factors can further exacerbate corneal endothelial injury; the combined effects of these factors may contribute to the development of postoperative complications such as corneal oedema, loss of corneal endothelial cells, corneal decompensation, and delayed recovery of visual function.Clarifying the mechanisms of PHACO-related corneal endothelial damage in patients with DM and summarising perioperative protective strategies will provide valuable guidance for the protection of the corneal endothelium and the prevention and treatment of related complications during the perioperative period of PHACO in patients with DM.
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基本信息:
中图分类号:R587.2;R779.66
引用信息:
[1]史乙彤,王琳,张培培,等.糖尿病患者白内障超声乳化术相关角膜内皮损伤机制及防护策略研究进展[J].山东医药,2026,66(07):170-174.
基金信息:
山东省医药卫生科技项目（202307020773）
2026-07-25
2026-07-25