增加质糖解促进近视通过组织素乳化近视
Xiaolei Lin1, Yi Lei1, Miaozhen Pan1
1State Key Laboratory of Ophthalmology, Optometry and Vision Science, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, Zhejiang, China; National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, Zhejiang, China.
Cell metabolism
|January 17, 2024
概括
质糖解和乳酸生产通过通过基因素乳化增加纤维细胞到肌纤维细胞转差 (FMT) 来促进近视. 抑制糖解或乳酸生产可以预防或减少近视的发展.
科学领域:
- 眼科医生 眼科 眼科
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 近视的进展与膜中的纤维细胞到肌纤维细胞转差 (FMT) 的不适应性有关.
- 膜缺氧与近视有关,但其确切的机制尚不清楚.
研究的目的:
- 调查质糖解和乳酸生产在近视发展中的作用.
- 阐明将缺氧,糖解和近视联系在一起的分子机制.
主要方法:
- 评估了小鼠和几内亚猪模型中的近视发展.
- 测量了质糖解,乳酸水平和纤维细胞到肌纤维细胞转差 (FMT).
- 研究了基因素乳化 (H3K18la) 和Notch1表达的作用.
主要成果:
- 低氧诱导了硬膜中的糖解和乳酸的增加,促进了FMT和近视.
- 抑制糖解或乳酸生产改善了近视.
- 通过H3K18la,质糖解-乳酸促进了近视,上调了Notch1.1.
- 增加糖分摄入量通过这种途径加剧了近视.
结论:
- 质糖解和乳酸生产是近视的关键驱动因素.
- 质糖解-乳酸盐-基因素乳化途径有助于近视的发病.
- 向质糖解可能为近视提供治疗策略.
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