中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (10): 2230-2231.doi: 10.4103/1673-5374.335801

• 观点:视神经损伤修复保护与再生 • 上一篇    下一篇

缺氧反应中视网膜神经节细胞的退化:缺氧诱导因子抑制,作为治疗靶点的新见解

  

  • 出版日期:2022-10-15 发布日期:2022-03-16

Degeneration of retinal ganglion cells in hypoxic responses: hypoxia-inducible factor inhibition, a new therapeutic insight

Deokho Lee, Hiromitsu Kunimi, Kazuno Negishi, Toshihide Kurihara   

  1. Department of Ophthalmology, Keio University School of Medicine, Shinanomachi, Shinjuku-ku, Japan
  • Online:2022-10-15 Published:2022-03-16
  • Contact: Toshihide Kurihara, MD, PhD, kurihara@z8.keio.jp.
  • Supported by:
    The present work was supported by Alcon Japan Research Grant (to TK). Furthermore, it was supported by Grants-in-Aid for Scientific Research (KAKENHI, number 18K09424 to TK, and 20K22692 to HK) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT). At last, it was supported by Bayer Academic Support (to HK).

摘要: https://orcid.org/0000-0002-5457-2720 (Toshihide Kurihara)

Abstract: Degeneration of retinal ganglion cells (RGCs) is one of the hallmarks of common optic neuropathies (Weinreb et al., 2014). Glaucoma, the most common optic neuropathy, is characterized by degeneration of RGCs. Acute angle-closure glaucoma is a serious ocular condition caused by a rapid increase in intraocular pressure (IOP) (Emanuel et al., 2014). One of the experimental models which could mimic this condition is a murine model of retinal ischemia/reperfusion (I/R) injury (Johnson and Tomarev, 2010). Retinal I/R injury can induce a rapid and transient elevation of IOP, which contributes to the degeneration of RGCs. Although understanding the pathophysiology of the degeneration of RGCs was considerably attempted, the major contributing pathways have not been yet elucidated (Calkins and Horner, 2012).