Evidence map›Paper›PMID 35955937›Full record

ArticleInternational journal of molecular sciences2022

SIG-1451, a Novel, Non-Steroidal Anti-Inflammatory Compound, Attenuates Light-Induced Photoreceptor Degeneration by Affecting the Inflammatory Process.

Yuki Kikuchi, Eriko Sugano, Shiori Yuki, Kitako Tabata, Yuka Endo, Yuya Takita, Reina Onoguchi, Taku Ozaki, Tomokazu Fukuda, Yoshihiro Takai and 10 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 46% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 4 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 4 institutions in 2 countries.

Yuki KikuchiLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.
Eriko SuganoLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.
Shiori YukiLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.
Kitako TabataLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.
Yuka EndoLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.
Yuya TakitaLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.
Reina OnoguchiLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.
Taku OzakiLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.ORCID 0000-0001-8183-5453
Tomokazu FukudaLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.
Yoshihiro TakaiRohto Pharmaceutical Co., Ltd., 6-5-4 Kunimidai, Kizugawa 619-0216, Kyoto, Japan.
Takahiro KuroseRohto Pharmaceutical Co., Ltd., 6-5-4 Kunimidai, Kizugawa 619-0216, Kyoto, Japan.
Koichi TanakaRohto Pharmaceutical Co., Ltd., 6-5-4 Kunimidai, Kizugawa 619-0216, Kyoto, Japan.
Yoichi HonmaRohto Pharmaceutical Co., Ltd., 6-5-4 Kunimidai, Kizugawa 619-0216, Kyoto, Japan.
Eduardo PerezSignum Biosciences, 4999 Pearl East Circle, Boulder, CO 80301, USA.ORCID 0000-0002-7112-6896
Maxwell StockSignum Biosciences, 4999 Pearl East Circle, Boulder, CO 80301, USA.
José R FernándezSignum Biosciences, 4999 Pearl East Circle, Boulder, CO 80301, USA.
Masanori TamuraSignum Biosciences, 4999 Pearl East Circle, Boulder, CO 80301, USA.
Michael VoronkovSignum Biosciences, 4999 Pearl East Circle, Boulder, CO 80301, USA.
Jeffry B StockDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544-1014, USA.
Hiroshi TomitaLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University Division of Science and Engineering, 4-3-5 Ueda, Morioka 020-8551, Iwate, Japan.ORCID 0000-0003-1051-2301
Iwate University · JPSignum Biosciences (United States) · USRohto Pharmaceutical (Japan) · JPPrinceton University · US

Funding

Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan 21K18278, 19H03807, 19K09945, and 21K09713
6 · The paper itself

Abstract

Age-related macular degeneration is a progressive retinal disease that is associated with factors such as oxidative stress and inflammation. In this study, we evaluated the protective effects of SIG-1451, a non-steroidal anti-inflammatory compound developed for treating atopic dermatitis and known to inhibit Toll-like receptor 4, in light-induced photoreceptor degeneration. SIG-1451 was intraperitoneally injected into rats once per day before exposure to 1000 lx light for 24 h; one day later, optical coherence tomography showed a decrease in retinal thickness, and electroretinogram (ERG) amplitude was also found to have decreased 3 d after light exposure. Moreover, SIG-1451 partially protected against this decrease in retinal thickness and increase in ERG amplitude. One day after light exposure, upregulation of inflammatory response-related genes was observed, and SIG-1451 was found to inhibit this upregulation. Iba-1, a microglial marker, was suppressed in SIG-1451-injected rats. To investigate the molecular mechanism underlying these effects, we used lipopolysaccharide (LPS)-stimulated rat immortalised Müller cells. The upregulation of C-C motif chemokine 2 by LPS stimulation was significantly inhibited by SIG-1451 treatment, and Western blot analysis revealed a decrease in phosphorylated I-κB levels. These results indicate that SIG-1451 indirectly protects photoreceptor cells by attenuating light damage progression, by affecting the inflammatory responses.

Indexed as

LipopolysaccharidesRetinal DegenerationAnimalsAnti-Inflammatory AgentsElectroretinographyLightPhotoreceptor Cells, VertebrateRatsRetinaAnti-Inflammatory AgentsLipopolysaccharidesage-related macular degenerationanti-inflammatory druglight-induced photoreceptor degenerationToll-like receptor 4

Identifiers

PMID35955937
PMCPMC9369167
OpenAlexW4295725710

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.