Hwang Ho Sik, Parfitt Geraint J, Brown Donald J, Jester James V
Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA, United States; Department of Ophthalmology, Chuncheon Sacred Heart Hospital, Hallym University, Korea.
Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA, United States.
Exp Eye Res. 2017 Oct;163:37-45. doi: 10.1016/j.exer.2017.02.008. Epub 2017 Feb 17.
This paper reviews our current understanding of age-related meibomian gland dysfunction (MGD) and the role of the nuclear receptor, peroxisome proliferator-activated receptor gamma (PPARγ), in the regulation of meibomian gland function, meibocyte differentiation and lipid synthesis. The studies suggest that PPARγ is a master regulator of meibocyte differentiation and function, whose expression and nuclear signaling coupled with meibocyte renewal is altered during aging, potentially leading to atrophy of the meibomian gland as seen in clinical MGD. Study of meibomian gland stem cells also suggest that there is a limited number of precursor meibocytes that provide progeny to the acini, that may be susceptible to exhaustion as occurs during aging and other environmental factors. Further study of pathways regulating PPARγ expression and function as well as meibocyte stem cell maintenance may provide clues to establishing cellular and molecular mechanisms underlying MGD and the development of novel therapeutic strategies to treating this disease.
本文综述了我们目前对年龄相关性睑板腺功能障碍（MGD）的理解，以及核受体过氧化物酶体增殖物激活受体γ（PPARγ）在睑板腺功能调节、睑板腺细胞分化和脂质合成中的作用。研究表明，PPARγ是睑板腺细胞分化和功能的主要调节因子，其表达和核信号传导与睑板腺细胞更新在衰老过程中发生改变，这可能导致临床MGD中所见的睑板腺萎缩。对睑板腺干细胞的研究还表明，为腺泡提供子代的前体睑板腺细胞数量有限，这些细胞可能在衰老和其他环境因素作用下易发生耗竭。进一步研究调节PPARγ表达和功能以及睑板腺干细胞维持的信号通路，可能为揭示MGD的细胞和分子机制以及开发治疗该疾病的新治疗策略提供线索。
