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Pathophysiology of Corneal Endothelial Cell Loss in Dry Eye Disease and Other Inflammatory Ocular Disorders
Ocular Immunology and Inflammation ( IF 3.3 ) Pub Date : 2021-10-22 , DOI: 10.1080/09273948.2021.1980808
Amardeep S Sekhon 1 , Bonnie He 2 , Alfonso Iovieno 3 , Sonia N Yeung 3
Affiliation  

ABSTRACT

Purpose

Dry eye disease (DED) and other inflammatory ocular disorders have been reported to be associated with decreased corneal endothelial cell density (CECD), however the mechanism of underlying endothelial cell loss remains unknown.

Methods

We conducted a comprehensive literature search of English-written publications on dry eye disease, corneal endothelial cell loss, Sjögren’s syndrome, and Graft Vs Host Disease (GVHD), to review the effects of DED and other inflammatory ocular surface conditions on CECD.

Results

A total of 78 studies were included in our study. Loss of corneal neurotrophic support, cytotoxic stress, and a heightened immune response, all of which may occur secondarily to a common causative agent such as inflammation, are major contributors to reduced CECD.

Conclusion

More studies are needed to determine how the interrelated pathways of altered corneal nerve function and upregulated expression of inflammatory activity influence corneal endothelial cell loss.



中文翻译:

干眼病和其他炎症性眼病中角膜内皮细胞丢失的病理生理学

摘要

目的

据报道,干眼病 (DED) 和其他炎症性眼部疾病与角膜内皮细胞密度 (CECD) 降低有关,但潜在内皮细胞丢失的机制仍然未知。

方法

我们对有关干眼病、角膜内皮细胞丢失、干燥综合征和移植物抗宿主病 (GVHD) 的英文出版物进行了全面的文献检索,以审查 DED 和其他炎症性眼表疾病对 CECD 的影响。

结果

我们的研究共纳入了 78 项研究。角膜神经营养支持的丧失、细胞毒性应激和免疫反应增强,所有这些都可能继发于炎症等常见病原体,是降低 CECD 的主要原因。

结论

需要更多的研究来确定角膜神经功能改变和炎症活性表达上调的相互关联途径如何影响角膜内皮细胞丢失。

更新日期:2021-10-22
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