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作 者:Yue Guan Juan Li Tao Zhan Jian-Wen Wang Jian-Bo Yu Lan Yang
机构地区:[1]Department of Ophthalmology, Affiliated Hongqi Hospital, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, China [2]Department of Endocrinology, Affiliated Hongqi Hospital, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, China [3]Department of Pathology, Affiliated Hongqi Hospital, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, China
出 处:《Chinese Medical Journal》2016年第16期2001-2004,共4页中华医学杂志(英文版)
基 金:The work was supported by a grant from Project of Science Foundation of Mudanjiang (No. G2012s0028).
摘 要:INTRODUCTION Glaucoma is a chronic progressive neurodegenerative disease and exhibits heterogeneity, polygenic inheritance, and incomplete penetrance. Primary open-angle glaucoma (POAG) is the most common form of glaucoma. Although the underlying etiology of POAG is unknown, there is evidence that genetic mutations are closely associated with this disease, Among myocilin (MYOC) mutations, Pro370Leu (P370L) is responsible for one of the most severe glaucoma phenotypes, However, the function of MYOC protein is still not well understood.INTRODUCTION Glaucoma is a chronic progressive neurodegenerative disease and exhibits heterogeneity, polygenic inheritance, and incomplete penetrance. Primary open-angle glaucoma (POAG) is the most common form of glaucoma. Although the underlying etiology of POAG is unknown, there is evidence that genetic mutations are closely associated with this disease, Among myocilin (MYOC) mutations, Pro370Leu (P370L) is responsible for one of the most severe glaucoma phenotypes, However, the function of MYOC protein is still not well understood.
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