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We began analyzing https://www.nature.com/articles/srep44873, but it redirected us to https://www.nature.com/articles/srep44873. The analysis below is for the second page.

Title[redir]:
KUS121, a VCP modulator, attenuates ischemic retinal cell death via suppressing endoplasmic reticulum stress | Scientific Reports
Description:
Ischemic neural damages cause several devastating diseases, including brain stroke and ischemic retinopathies, and endoplasmic reticulum (ER) stress has been proposed to be the underlying mechanism of the neuronal cell death of these conditions. We previously synthesized Kyoto University substances (KUSs) as modulators of valosin-containing protein (VCP); KUSs inhibit VCP ATPase activity and protect cells from different cell death-inducing insults. Here, we examined the efficacy of KUS121 in a rat model of retinal ischemic injury. Systemic administration of KUS121 to rats with ischemic retinal injury significantly suppressed inner retinal thinning and death of retinal ganglion and amacrine cells, with a significant functional maintenance of visual functions, as judged by electroretinography. Furthermore, intravitreal injection of KUS121, which is the clinically preferred route of drug administration for retinal diseases, appeared to show an equal or better neuroprotective efficacy in the ischemic retina compared with systemic administration. Indeed, induction of the ER stress marker C/EBP homologous protein (CHOP) after the ischemic insult was significantly suppressed by KUS121 administration. Our study suggests VCP modulation by KUS as a promising novel therapeutic strategy for ischemic neuronal diseases.

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Keywords {🔍}

retinal, ischemic, kus, injury, control, cell, layer, article, group, cells, rats, thickness, retina, pubmed, google, scholar, vcp, insult, fig, doi, rgcs, ganglion, ischemia, days, death, effects, outer, neuroprotective, images, nuclear, cas, rat, kustreated, research, stress, model, nature, significantly, bwave, protein, number, diseases, treatment, test, treated, groups, sections, rgc, chop, error,

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nature portfolio privacy policy nature genetics 36 nature advertising social media monosodium iodoacetate-induced osteoarthritis pressure-induced ischaemia-reperfusion insult index 0/ reprints author information authors cell death-inducing insults pct/jp2011/067320&pct/jp2011/073160 japan research foundation er stress-induced molecule author correspondence facial nerve research er stress-reducing activities integrated medical bio-imaging nampt-dependent nad+ salvage transgenic thy1-gfp rat proteasome-mediated protein degradation joint research project flat-mounted retinal imaging light-emitting diode stimulator ganglion cell complex fewer tunel-positive cells thy1-green fluorescent protein decreased b-wave amplitude investigator-initiated clinical trial fewer chop-positive rgcs ivt-kus121–treated group compared flat-mounted retinal images ischemia-reperfusion injured retina flat-mounted retinas treated ganglion cell layer profound anti-apoptotic effect retinal ischemia-reperfusion injury permissions 5 mg/kg body weight colorimetric-tdt enzyme assessed b-wave amplitudes vcp/p97 aaa-atpase neuronal cell death human subjects subjected anti-cleaved caspase-3 antibody induces cell death necrotic cell death gfp-positive rgc numbers japan national society

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         description:Ischemic neural damages cause several devastating diseases, including brain stroke and ischemic retinopathies, and endoplasmic reticulum (ER) stress has been proposed to be the underlying mechanism of the neuronal cell death of these conditions. We previously synthesized Kyoto University substances (KUSs) as modulators of valosin-containing protein (VCP); KUSs inhibit VCP ATPase activity and protect cells from different cell death-inducing insults. Here, we examined the efficacy of KUS121 in a rat model of retinal ischemic injury. Systemic administration of KUS121 to rats with ischemic retinal injury significantly suppressed inner retinal thinning and death of retinal ganglion and amacrine cells, with a significant functional maintenance of visual functions, as judged by electroretinography. Furthermore, intravitreal injection of KUS121, which is the clinically preferred route of drug administration for retinal diseases, appeared to show an equal or better neuroprotective efficacy in the ischemic retina compared with systemic administration. Indeed, induction of the ER stress marker C/EBP homologous protein (CHOP) after the ischemic insult was significantly suppressed by KUS121 administration. Our study suggests VCP modulation by KUS as a promising novel therapeutic strategy for ischemic neuronal diseases.
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      headline:KUS121, a VCP modulator, attenuates ischemic retinal cell death via suppressing endoplasmic reticulum stress
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