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Meibocyte differentiation and renewal: Insights into novel mechanisms of meibomian gland dysfunction (MGD).睑板腺细胞分化与更新:睑板腺功能障碍(MGD)新机制的见解
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本文引用的文献

1
Intracrine activity involving NAD-dependent circadian steroidogenic activity governs age-associated meibomian gland dysfunction.内源性活动涉及 NAD 依赖性昼夜节律性甾体生成活性,可控制与年龄相关的睑板腺功能障碍。
Nat Aging. 2022 Feb;2(2):105-114. doi: 10.1038/s43587-021-00167-8. Epub 2022 Feb 10.
2
Periplocin ameliorates mouse age-related meibomian gland dysfunction through up-regulation of Na/K-ATPase via SRC pathway.千里光诺林通过 SRC 通路上调 Na/K-ATP 酶改善小鼠年龄相关性睑板腺功能障碍。
Biomed Pharmacother. 2022 Feb;146:112487. doi: 10.1016/j.biopha.2021.112487. Epub 2021 Dec 6.
3
Expression of Acyl-CoA wax-alcohol acyltransferase 2 (AWAT2) by human and rabbit meibomian glands and meibocytes.人及兔眼睑板腺和眼板腺细胞中酰基辅酶 A 蜡醇酰基转移酶 2(AWAT2)的表达。
Ocul Surf. 2022 Jan;23:60-70. doi: 10.1016/j.jtos.2021.11.010. Epub 2021 Nov 24.
4
Spontaneous acinar and ductal regrowth after meibomian gland atrophy induced by deletion of FGFR2 in a mouse model.在小鼠模型中,通过 FGFR2 的缺失诱导的睑板腺萎缩后的自发腺泡和导管再生。
Ocul Surf. 2022 Oct;26:300-309. doi: 10.1016/j.jtos.2021.11.005. Epub 2021 Nov 16.
5
Alteration in meibum lipid composition and subjective symptoms due to aging and meibomian gland dysfunction.由于衰老和睑板腺功能障碍导致的睑脂脂质组成改变和主观症状。
Ocul Surf. 2022 Oct;26:310-317. doi: 10.1016/j.jtos.2021.10.003. Epub 2021 Oct 16.
6
Effects of Aging on Human Meibum.人眼睑板腺功能随增龄变化的研究进展
Invest Ophthalmol Vis Sci. 2021 Sep 2;62(12):23. doi: 10.1167/iovs.62.12.23.
7
Quantitative analysis of morphological and functional features in Meibography for Meibomian Gland Dysfunction: Diagnosis and Grading.睑板腺功能障碍的睑板造影术形态学和功能特征的定量分析:诊断与分级
EClinicalMedicine. 2021 Sep 11;40:101132. doi: 10.1016/j.eclinm.2021.101132. eCollection 2021 Oct.
8
Epithelial stem cell homeostasis in Meibomian gland development, dysfunction, and dry eye disease.睑板腺发育、功能障碍和干眼症中的上皮干细胞稳态。
JCI Insight. 2021 Oct 22;6(20):e151078. doi: 10.1172/jci.insight.151078.
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Inhibition of ceramide de novo synthesis ameliorates meibomian gland dysfunction induced by SCD1 deficiency.抑制神经酰胺从头合成可改善 SCD1 缺乏诱导的睑板腺功能障碍。
Ocul Surf. 2021 Oct;22:230-241. doi: 10.1016/j.jtos.2021.08.016. Epub 2021 Aug 30.
10
Quantifying Meibomian Gland Morphology Using Artificial Intelligence.使用人工智能定量测量睑板腺形态。
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睑板腺干细胞/祖细胞:寻找腺体更新。

Meibomian gland stem/progenitor cells: The hunt for gland renewal.

机构信息

State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong, China.

Department of Ophthalmology, University of Missouri, Columbia, MO, USA.

出版信息

Ocul Surf. 2023 Jul;29:497-507. doi: 10.1016/j.jtos.2023.07.004. Epub 2023 Jul 6.

DOI:10.1016/j.jtos.2023.07.004
PMID:37422152
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10528929/
Abstract

Meibomian glands (MGs) secrete lipid (meibum) onto the ocular surface to form the outermost layer of the tear film. Proper meibum secretion is essential for stabilizing the tear film, reducing aqueous tear evaporation, and maintaining the homeostasis of the ocular surface. Atrophy of MG as occurs with aging, leads to reduction of meibum secretion, loss of ocular surface homeostasis and evaporative dry eye disease (EDED). Since MGs are holocrine glands, secretion of meibum requires continuous self-renewal of lipid-secreting acinar meibocytes by stem/progenitor cells, whose proliferative potential is dramatically reduced with age leading to MG atrophy and an age-related meibomian gland dysfunction (ARMGD). Understanding the cellular and molecular mechanisms regulating meibocyte stem/progenitor cell maintenance and renewal may provide novel approaches to regenerating MG and treating EDED. Towards that end, recent label retaining cell and lineage-tracing experiments as well as knock-out transgenic mouse studies have begun to identify the location and identities of meibocyte progenitor cells and potential growth and transcription factors that may regulate meibocyte renewal. In addition, recent reports have shown that ARMGD may be reversed by novel therapeutics in mice. Herein, we discuss our current understanding of meibocyte stem/progenitor cells and the hunt for gland renewal.

摘要

睑板腺(MGs)分泌脂质(睑脂)到眼表面,形成泪膜的最外层。适当的睑脂分泌对于稳定泪膜、减少水样泪液蒸发和维持眼表面的内稳态至关重要。随着年龄的增长,MG 萎缩会导致睑脂分泌减少、眼表面内稳态丧失和蒸发性干眼症(EDED)。由于 MGs 是全浆分泌腺,因此睑脂的分泌需要由干细胞/祖细胞不断自我更新脂分泌的腺泡型 meibocytes,其增殖潜力随着年龄的增长而显著降低,导致 MG 萎缩和与年龄相关的睑板腺功能障碍(ARMGD)。了解调节 meibocyte 干细胞/祖细胞维持和更新的细胞和分子机制可能为再生 MG 和治疗 EDED 提供新的方法。为此,最近的标记保留细胞和谱系追踪实验以及敲除转基因小鼠研究开始确定 meibocyte 祖细胞的位置和身份,以及可能调节 meibocyte 更新的生长和转录因子。此外,最近的报告表明,新型治疗药物可能逆转 ARMGD。在此,我们讨论我们对 meibocyte 干细胞/祖细胞的现有理解和寻找腺体更新的方法。