Evidence map›Paper›PMID 41752067›Full record

ArticleInternational journal of molecular sciences2026

Pyrroloquinoline Quinone Protects Against Light-Induced Retinal Damage in Association with the Suppression of c-Fos Signalling.

Hinata Ozawa, Eriko Sugano, Kitako Tabata, Taira Kakizaki, Akimune Sato, Yoshihiro Takai, Kohei Sone, Miwako Shidomi, Yuki Ishii, Akito Saito and 5 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Hinata OzawaLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.
Eriko SuganoLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.ORCID 0000-0001-6732-717X
Kitako TabataLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.ORCID 0000-0001-7048-917X
Taira KakizakiLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.
Akimune SatoLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.
Yoshihiro TakaiEye Care Product Development Division, ROHTO Pharmaceutical Co., Ltd., 6-5-4, Kunimidai, Kizugawa, Kyoto 619-0216, Japan.
Kohei SoneEye Care Product Development Division, ROHTO Pharmaceutical Co., Ltd., 6-5-4, Kunimidai, Kizugawa, Kyoto 619-0216, Japan.
Miwako ShidomiHealth Skin Science Business Planning Division, ROHTO Pharmaceutical Co., Ltd., 20F Shiodome Bldg. 1-2-20, Kaigan, Minato-ku, Tokyo 105-0022, Japan.
Yuki IshiiHealth Skin Science Business Planning Division, ROHTO Pharmaceutical Co., Ltd., 20F Shiodome Bldg. 1-2-20, Kaigan, Minato-ku, Tokyo 105-0022, Japan.
Akito SaitoLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.
Kentaro TotukaLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.
Taku OzakiLaboratory of Biochemistry, Molecular Medical Science, Division of Agriculture, Iwate University, 3-18-33 Ueda, Morioka 020-8550, Japan.ORCID 0000-0001-8183-5453
Tomokazu FukudaLaboratory of Cell Engineering and Molecular Genetics, Molecular Medical Science, Division of Agriculture, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.ORCID 0000-0001-8456-0483
Lanlan BaiLaboratory of Cell Engineering and Molecular Genetics, Molecular Medical Science, Division of Agriculture, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.ORCID 0000-0002-2414-3247
Hiroshi TomitaLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Division of Science and Engineering, Iwate University, 4-3-5 Ueda, Morioka 020-8551, Japan.ORCID 0000-0003-1051-2301

Funding

Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology, Japan 21K09713Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology, Japan 21K18278Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology, Japan 22H00579Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology, Japan 22K09760
6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is a progressive retinal disorder characterised by oxidative stress and inflammation. Although pyrroloquinoline quinone (PQQ) has been reported to exert neuroprotective effects, its specific efficacy in in vivo models of AMD pathophysiology has not yet been elucidated. In this study, we evaluated the protective effects of PQQ against all-trans-retinal (ATR)-induced cytotoxicity in ARPE-19 cells and light-induced photoreceptor degeneration in rats. Pretreatment of ARPE-19 cells with PQQ dose-dependently mitigated ATR-induced cytotoxicity. In the in vivo model, rats received a single intraperitoneal injection of PQQ (2 or 5 mg/kg) 1 h prior to 1000-lux light exposure. Retinal function and morphology were evaluated by electroretinography and haematoxylin-eosin staining, respectively. The 5 mg/kg PQQ group retained significantly greater retinal function than the vehicle group at 3 days postexposure and demonstrated significant preservation of the outer nuclear layer at 7 days postexposure, indicating the suppression of photoreceptor cell death. Western blot analysis detected the dose-dependent suppression of light-induced c-Fos upregulation following PQQ treatment. These findings suggest that the protective effect of PQQ against phototoxic damage is associated with the suppression of c-Fos signalling, thus lending support to the further investigation of PQQ as a potential therapeutic agent for AMD.

Indexed as

LightPQQ CofactorProto-Oncogene Proteins c-fosRetinaRetinal DegenerationSignal TransductionAnimalsCell LineElectroretinographyHumansMaleOxidative StressRatsPQQ CofactorProto-Oncogene Proteins c-fosage-related macular degenerationc-Foslight-induced photoreceptor degenerationoxidative stresspAktphotoreceptor cellpyrroloquinoline quinoneretinal pigment epithelium cell

Identifiers

PMID41752067
PMCPMC12941150

What OpenQuestion holds

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Registered trials

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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.