Neural degeneration in the retina of the streptozotocin-induced type 1 diabetes model

Yoko Ozawa, Toshihide Kurihara, Mariko Sasaki, Norimitsu Ban, Kenya Yuki, Shunsuke Kubota, Kazuo Tsubota

研究成果: Review article査読

61 被引用数 (Scopus)

抄録

Diabetic retinopathy, a vision-threatening disease, has been regarded as a vascular disorder. However, impaired oscillatory potentials (OPs) in the electroretinogram (ERG) and visual dysfunction are recorded before severe vascular lesions appear. Here, we review the molecular mechanisms underlying the retinal neural degeneration observed in the streptozotocin-(STZ-) induced type 1 diabetes model. The renin-angiotensin system (RAS) and reactive oxygen species (ROS) both cause OP impairment and reduced levels of synaptophysin, a synaptic vesicle protein for neurotransmitter release, most likely through excessive protein degradation by the ubiquitin-proteasome system. ROS also decrease brain-derived neurotrophic factor (BDNF) and inner retinal neuronal cells. The influence of both RAS and ROS on synaptophysin suggests that RAS-ROS crosstalk occurs in the diabetic retina. Therefore, suppressors of RAS or ROS, such as angiotensin II type 1 receptor blockers or the antioxidant lutein, respectively, are potential candidates for neuroprotective and preventive therapies to improve the visual prognosis.

本文言語English
論文番号108328
ジャーナルExperimental Diabetes Research
2011
DOI
出版ステータスPublished - 2011

ASJC Scopus subject areas

  • 内分泌学、糖尿病および代謝内科学

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