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Recent advances in genetically modified animal models of glaucoma and their roles in drug repositioning
  1. Chikako Harada,
  2. Atsuko Kimura,
  3. Xiaoli Guo,
  4. Kazuhiko Namekata,
  5. Takayuki Harada
  1. Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan
  1. Correspondence to Professor Takayuki Harada, Visual Research Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan; harada-tk{at}igakuken.or.jp

Abstract

Glaucoma is one of the leading causes of vision loss in the world. Currently, pharmacological intervention for glaucoma therapy is limited to eye drops that reduce intraocular pressure (IOP). Recent studies have shown that various factors as well as IOP are involved in the pathogenesis of glaucoma, especially in the subtype of normal tension glaucoma. To date, various animal models of glaucoma have been established, including glutamate/aspartate transporter knockout (KO) mice, excitatory amino acid carrier 1 KO mice, optineurin E50K knock-in mice, DBA/2J mice and experimentally induced models. These animal models are very useful for elucidating the pathogenesis of glaucoma and for identifying potential therapeutic targets. However, each model represents only some aspects of glaucoma, never the whole disease. This review will summarise the benefits and limitations of using disease models of glaucoma and recent basic research in retinal protection using existing drugs.

  • glaucoma
  • degeneration
  • drugs
  • experimental – animal models
  • experimental – laboratory

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0

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Footnotes

  • Contributors All the authors wrote the manuscript, prepared the figure and tables, and read and approved the manuscript.

  • Funding This work was supported by JSPS KAKENHI JP16K11308 (CH), JP17K07123 (AK), JP16K07076 (XG), JP16K08635 (KN), JP15H04999 and JP18K19625 (TH), the Mitsui Life Social Welfare Foundation and the Takeda Science Foundation (TH).

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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