Scleral hypoxia is a target for myopia control

Hao Wu(Wenzhou Medical University), Wei Chen(Chinese Academy of Sciences), Fei Zhao(Wenzhou Medical University), Qingyi Zhou(Wenzhou Medical University), Peter S. Reinach(Wenzhou Medical University), Lili Deng(Chinese Academy of Sciences), Li Ma(Wenzhou Medical University), Shumeng Luo(Chinese Academy of Sciences), Nethrajeith Srinivasalu(Wenzhou Medical University), Miaozhen Pan(Wenzhou Medical University), Yang Hu(Wenzhou Medical University), Xiaomeng Pei(Wenzhou Medical University), Jing Sun(Wenzhou Medical University), Ran Ren(Wenzhou Medical University), Yinghui Xiong(Wenzhou Medical University), Zhonglou Zhou(Wenzhou Medical University), Sen Zhang(Wenzhou Medical University), Geng Tian(Tsinghua University), Jianhuo Fang(Tsinghua University), Lina Zhang(Tsinghua University), Jidong Lang(Tsinghua University), Deng Wu(Chinese Academy of Sciences), Changqing Zeng(Chinese Academy of Sciences), Jia Qu(Wenzhou Medical University), Xiangtian Zhou(Wenzhou Medical University)
Proceedings of the National Academy of Sciences
July 9, 2018
Cited by 509Open Access
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Abstract

) promoted myofibroblast transdifferentiation with down-regulation of type I collagen in human scleral fibroblasts. Importantly, the antihypoxia drugs salidroside and formononetin down-regulated HIF-1α expression as well as the phosphorylation levels of eIF2α and mTOR, slowing experimental myopia progression without affecting normal ocular growth in guinea pigs. Furthermore, eIF2α phosphorylation inhibition suppressed experimental myopia, whereas mTOR phosphorylation induced myopia in normal mice. Collectively, these findings defined an essential role of hypoxia in scleral ECM remodeling and myopia development, suggesting a therapeutic approach to control myopia by ameliorating hypoxia.


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