中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (6): 1221-1222.doi: 10.4103/1673-5374.300445

• 观点:视神经损伤修复保护与再生 • 上一篇    下一篇

诱导型一氧化氮合酶抑制剂1400W可作为治疗视网膜疾病的潜在方法

  

  • 出版日期:2021-06-15 发布日期:2020-12-31

The inducible nitric oxide synthase-inhibitor 1400W as a potential treatment for retinal diseases

Sven Schnichels*, Stephanie C. Joachim   

  1. University Eye Hospital Tübingen, Centre for Ophthalmology, Tübingen, Germany (Schnichels S)
    Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, Bochum, Germany (Joachim SC)
  • Online:2021-06-15 Published:2020-12-31
  • Contact: Sven Schnichels, PhD,sven.schnichels@med.uni-tuebingen.de.
  • Supported by:
    We thank all the collaborators and coauthors who thereby contributed to this perspective article, especially José Hurst and Ana Mueller-Buehl. We also thank Sami Ullah and Teresa Tsai for their support concerning the figures as well as for critical proof reading.  

    This work was supported in part by the set Stiftung.

摘要: https://orcid.org/0000-0002-2385-5517 (Sven Schnichels)

Abstract: The overproduction of reactive oxygen species is defined as oxidative stress. While deprived oxygen supply in tissues is known as hypoxia. These mechanisms contribute to the pathogenesis of several retinal diseases, like glaucoma, age-related macular degeneration (AMD), and retinal ischemia. Glaucoma is a neurodegenerative disease defined by a progressive loss of retinal ganglion cells (RGCs) and their axons causing visual field defects, which ultimately leads to blindness. While AMD pathogenesis is further characterized by soft drusen, it involves the retinal pigment epithelium and the Bruch’s membrane - choroid complex. AMD is a disease finally leading to death of the photoreceptors, especially in the macula region, resulting in central vision loss. The pathomechanisms of both diseases are not yet fully understood, but oxidative as well as hypoxic stresses seem to play a crucial. Moreover, hypoxia is also an inducer of oxidative stress by causing cellular stress, followed by mitochondrial stress, in neurodegenerative retinal diseases. In experimental models of retinal degeneration numerous triggers of cell death have been identified, including genetic mutations, intracellularly elevated calcium levels, endoplasmic reticulum stress, as well as hypoxia, and oxidative stress (Grossniklaus et al., 2010; Pang and Clark, 2020).