睑板腺萎缩危险因素的研究进展

doi:10.3877/cma.j.issn.2095-2007.2026.02.009

睑板腺功能障碍(MGD)是引起眼干、烧灼感、畏光及迎风流泪等常见症状的主要原因之一。其中，睑板腺萎缩作为MGD的重要病理表型，可导致患者出现更为严重的眼部不适。近年来，受不良用眼习惯、环境变化及生活方式等多重因素影响，睑板腺萎缩的整体患病率持续攀升，发病群体有年轻化趋势，目前缺乏逆转腺体损伤和促进萎缩睑板腺组织再生的有效治疗手段。衰老、全身性疾病、眼部慢性炎症、药物影响、环境刺激及不良用眼行为等多种危险因素可参与并加速睑板腺萎缩的发生与进展。本文中笔者就国内外睑板腺萎缩危险因素的研究进展进行综述，旨在为其发病机制研究及临床治疗提供新思路。

关键词: 睑板腺萎缩, 睑板腺功能障碍, 危险因素

Meibomian gland dysfunction (MGD) is one of the leading causes of common ocular symptoms including dry eye, burning sensation, photophobia and epiphora induced by wind. As a crucial pathological phenotype of MGD, meibomian gland atrophy can trigger more severe ocular discomfort in patients. In recent years, affected by multiple factors such as adverse eye habits, environmental changes and unhealthy lifestyles, the overall prevalence of meibomian gland atrophy has been rising steadily. Clinically, its affected population shows a distinct younger-onset trend. At present, there is a lack of curative therapeutic strategies that can effectively reverse glandular damage and promote the tissue regeneration of atrophic meibomian glands. A variety of risk factors, including aging, systemic diseases, chronic ocular inflammation, medication effects, environmental irritation and unhealthy ocular behaviors, also participate in and accelerate the occurrence and progression of meibomian gland atrophy. The research progress on risk factors of meibomian gland atrophy at home and abroad were reviewed, aiming to provide novel insights for the research on its pathogenesis and clinical treatment.

Key words: Meibomian gland atrophy, Meibomian gland dysfunction, Risk factors

表1 雄激素及雌激素对睑板腺功能影响的作用机制

第一作者	研究对象	干预方式	实验类别	作用机制
Sullivan等^[14]	去雄兔	19-去甲睾酮	动物实验	通过影响睑板腺脂质分布、调节脂质组成发挥作用
Schirra等^[16]	雄激素		动物实验	上调关键脂肪酶的信使核糖核酸水平，调控转录因子固醇调节元件结合蛋白1/2的编码基因，调节脂质合成
Sahin等^[17]	睑板腺腺泡上皮细胞	二氢睾酮	细胞实验	抑制脂多糖诱导的睑板腺腺泡上皮细胞中白细胞介素-6、白细胞介素-8、白细胞介素-1β及血管内皮生长因子-A等促炎细胞因子分泌；显著抑制睑板腺腺泡上皮细胞中多种免疫相关基因的表达
Suzuki等^[19]	鼠睑板腺		实验研究	雌激素下调环磷酸腺苷信号传导途径，影响睑板腺细胞增殖
李联祥等^[20]	人眼睑板腺		基础实验	快速非基因调节效应：性激素与膜受体结合，快速调节细胞功能；慢速基因表达调节：性激素与胞浆或胞核受体结合，调控腺体相关基因表达

表1 雄激素及雌激素对睑板腺功能影响的作用机制

第一作者	研究对象	干预方式	实验类别	作用机制
Sullivan等^[14]	去雄兔	19-去甲睾酮	动物实验	通过影响睑板腺脂质分布、调节脂质组成发挥作用
Schirra等^[16]	雄激素		动物实验	上调关键脂肪酶的信使核糖核酸水平，调控转录因子固醇调节元件结合蛋白1/2的编码基因，调节脂质合成
Sahin等^[17]	睑板腺腺泡上皮细胞	二氢睾酮	细胞实验	抑制脂多糖诱导的睑板腺腺泡上皮细胞中白细胞介素-6、白细胞介素-8、白细胞介素-1β及血管内皮生长因子-A等促炎细胞因子分泌；显著抑制睑板腺腺泡上皮细胞中多种免疫相关基因的表达
Suzuki等^[19]	鼠睑板腺		实验研究	雌激素下调环磷酸腺苷信号传导途径，影响睑板腺细胞增殖
李联祥等^[20]	人眼睑板腺		基础实验	快速非基因调节效应：性激素与膜受体结合，快速调节细胞功能；慢速基因表达调节：性激素与胞浆或胞核受体结合，调控腺体相关基因表达

表2 高血糖对睑板腺功能影响的作用机制

第一作者	研究对象	实验类别	作用机制	研究结论
Ding等^[29]	睑板腺腺泡上皮细胞	实验研究	胰岛素依赖胰岛素样生长因子-1受体激活睑板腺腺泡上皮细胞中的磷酸化蛋白激酶B，进而激活蛋白激酶B信号通路，调控腺体细胞增殖与脂质积累；高血糖显著改变胰岛素样生长因子-1信号通路相关蛋白表达	揭示了在胰岛素抵抗或缺乏时，高血糖对睑板腺腺泡上皮细胞的直接调控机制
Guo等^[27]	糖尿病小鼠	动物实验	糖尿病小鼠睑板腺内活性氧水平随病程递增，过量活性氧会破坏线粒体结构与功能；晚期糖基化终产物则会引发并加剧氧化应激，造成睑板腺损伤	证实氧化应激是糖尿病状态下睑板腺损伤的重要机制

表2 高血糖对睑板腺功能影响的作用机制

第一作者	研究对象	实验类别	作用机制	研究结论
Ding等^[29]	睑板腺腺泡上皮细胞	实验研究	胰岛素依赖胰岛素样生长因子-1受体激活睑板腺腺泡上皮细胞中的磷酸化蛋白激酶B，进而激活蛋白激酶B信号通路，调控腺体细胞增殖与脂质积累；高血糖显著改变胰岛素样生长因子-1信号通路相关蛋白表达	揭示了在胰岛素抵抗或缺乏时，高血糖对睑板腺腺泡上皮细胞的直接调控机制
Guo等^[27]	糖尿病小鼠	动物实验	糖尿病小鼠睑板腺内活性氧水平随病程递增，过量活性氧会破坏线粒体结构与功能；晚期糖基化终产物则会引发并加剧氧化应激，造成睑板腺损伤	证实氧化应激是糖尿病状态下睑板腺损伤的重要机制

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Advances on the risk factors for meibomian gland atrophy

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Advances on the risk factors for meibomian gland atrophy