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2017 ; 12
(8
): 1252-1255
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Modulation of valosin-containing protein by Kyoto University Substances (KUS) as
a novel therapeutic strategy for ischemic neuronal diseases
#MMPMID28966635
Hata M
; Ikeda HO
Neural Regen Res
2017[Aug]; 12
(8
): 1252-1255
PMID28966635
show ga
Retinal ischemia causes several vision-threatening diseases, including diabetic
retinopathy, retinal artery occlusion, and retinal vein occlusion. Intracellular
adenosine triphosphate (ATP) depletion and subsequent induced endoplasmic
reticulum (ER) stress are proposed to be the underlying mechanisms of ischemic
retinal cell death. Recently, we found that a naphthalene derivative can inhibit
ATPase activity of valosin-containing protein, universally expressed within
various types of cells, including retinal neural cells, with strong
cytoprotective activity. Based on the chemical structure, we developed novel
valosin-containing protein modulators, Kyoto University Substances (KUSs), that
not only inhibit intracellular ATP depletion, but also ameliorate ER stress.
Suppressing ER stress by KUSs is associated with neural cell survival in animal
models of several neurodegenerative diseases, such as glaucoma and retinal
degeneration. Given that a major pathology of ischemic retinal diseases, other
than intracellular ATP depletion, is ER stress-induced cell death, KUSs may
provide a novel strategy for cell protection in ischemic conditions. Hence, we
investigated the efficacy of KUS121 in a rat model of retinal ischemic injury.
Intravitreal injections of KUS121, which is clinically preferable route of drug
administration in retinal diseases, significantly suppressed inner retinal
thinning and retinal cell death, and maintained visual functions.
Valosin-containing protein modulation by KUS is a promising novel therapeutic
strategy for ischemic retinal diseases.