Interaction of ductal obstruction and glandular dropout in the pathogenesis of meibomian gland dysfunction  

作　　者：Ren Liu Jianwen Xue Jiaxu Han Jing Li Ziyan Chen Lingyi Liang 刘仁;薛建文;韩佳栩;李晶;陈子沿;梁凌毅(State Key Laboratory of Ophthalmology,Zhongshan Ophthalmic Center,Sun Yat-sen University,Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science,Guangzhou 510060,China)

机构地区：[1]State Key Laboratory of Ophthalmology,Zhongshan Ophthalmic Center,Sun Yat-sen University,Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science,Guangzhou 510060,China

出　　处：《Eye Science》2024年第3期190-205,共16页眼科学报（英文版）

基　　金：supported by the National Natural Science Foundation of China(82371021,82201142);the Science Foundation of Guangdong Province(2023A1515012336,2023A1515010091,2023A1515030238).

摘　　要：Meibomian gland dysfunction(MGD)manifests through two main clinical presentations,characterized by the meibomian gland(MG)ductal obstruction or acinar dropout.While previous research has predominantly associated MGD pathogenesis with hyperkeratinization-related MG ductal obstruction and subsequent acinar atrophy,recent cases have shown significant functional acinar loss in the absence of apparent ductal keratinization or blockage.The deterioration of either MG obstruction or dropout exacerbates the condition of the other,suggesting an independent yet interconnected relationship that perpetuates the vicious cycle of MGD.Understanding the distinct pathological features of MG obstruction and dropout is crucial for delineating their etiology and identifying targeted therapeutic strategies.This review explores the nuanced interrelations of MG obstruction and dropout,elucidating potential pathological mechanisms to establish a foundation for early MGD diagnosis and intervention.

关 键 词：Meibomian gland dysfunction Hyperkeratinization Inflammation PROGENITOR PPARγ. 

分 类 号：R77[医药卫生—眼科]