和歌山研讨会：过氧化物酶体增殖物激活受体-γ（PPARγ）与睑板腺功能障碍。
Wakayama Symposium: Peroxisome proliferator-activated receptor-gamma (PPARγ) and meibomian gland dysfunction.
机构信息
The Gavin Herbert Eye Institute, University of California Irvine, Irvine, California, USA.
出版信息
Ocul Surf. 2012 Oct;10(4):224-9. doi: 10.1016/j.jtos.2012.07.001. Epub 2012 Jul 25.
Recently we have shown that mouse and human meibomian glands undergo specific age-related changes, including decreased acinar cell proliferation, acinar atrophy, and altered peroxisome proliferator-activated receptor gamma (PPARγ) localization from cytoplasmic-vesicular/nuclear in young mice and humans to nuclear in old mice and humans. Since PPARγ is a lipid-sensitive, nuclear receptor implicated in regulating adipocyte and sebocyte differentiation and lipogenesis, our findings suggest that PPARγ may be involved in modulating meibomian gland differentiation during aging. Based on these findings, we propose that aging of the meibomian gland results in downregulation of PPARγ, leading to decreased meibocyte differentiation and lipid synthesis, gland atrophy, and a hyposecretory meibomian gland dysfunction.
最近，我们发现人和小鼠的睑板腺会发生特定的年龄相关性变化，包括细胞增殖减少、腺泡萎缩以及过氧化物酶体增殖物激活受体 γ（PPARγ）的定位改变，从年轻小鼠和人体内的细胞质-小泡/核转变成老年小鼠和人体内的核。由于 PPARγ 是一种对脂类敏感的核受体，与调节脂肪细胞和皮脂细胞分化以及脂肪生成有关，我们的研究结果表明，PPARγ 可能参与调节衰老过程中的睑板腺分化。基于这些发现，我们提出，睑板腺的衰老导致 PPARγ 的下调，导致类睑板腺细胞分化和脂质合成减少、腺泡萎缩以及分泌不足的睑板腺功能障碍。
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