In one paragraphArticle in FEBS open bio, 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
7 authors.
Amanda Alves NascimentoLaboratory Neurobiology of the retina, Biology Institute, Department of Neurobiology and Program of Neurosciences, Fluminense Federal University, Rio de Janeiro, Brazil.ORCID https://orcid.org/0000-0003-2729-9324 Danniel Pereira-FigueiredoLaboratory Neurobiology of the retina, Biology Institute, Department of Neurobiology and Program of Biomedical Sciences, Fluminense Federal University, Rio de Janeiro, Brazil.
Gabriella Grossi de Lima DiasLaboratory Neurobiology of the retina, Biology Institute, Department of Neurobiology and Program of Neurosciences, Fluminense Federal University, Rio de Janeiro, Brazil.ORCID https://orcid.org/0009-0002-1957-6467 Gabriel Ferreira Dos SantosLaboratory Neurobiology of the retina, Biology Institute, Department of Neurobiology and Program of Biomedical Sciences, Fluminense Federal University, Rio de Janeiro, Brazil.
Mariana Rodrigues PereiraChemical Signaling Laboratory, Biology Institute, Department of Neurobiology, Program of Neurosciences and Program in Science and Biotechnology, Fluminense Federal University, Rio de Janeiro, Brazil.ORCID https://orcid.org/0000-0001-5579-992X Rafael BritoLaboratory of Neuronal Physiology and Pathology, Department of Molecular and Cellular Biology, and Graduate Program of Neurosciences, Institute of Biology, Fluminense Federal University, Rio de Janeiro, Brazil.ORCID https://orcid.org/0000-0002-7070-3348 Karin C CalazaLaboratory Neurobiology of the retina, Biology Institute, Department of Neurobiology and Program of Neurosciences, Fluminense Federal University, Rio de Janeiro, Brazil.ORCID https://orcid.org/0000-0003-1199-1826 Funding
Conselho Nacional de Desenvolvimento Científico e Tecnológico 304410/2019-5Conselho Nacional de Desenvolvimento Científico e Tecnológico 316553/2023-9Conselho Nacional de Desenvolvimento Científico e Tecnológico 403325/2023-4Conselho Nacional de Desenvolvimento Científico e Tecnológico 409204/2024-2Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E-26/010.0022221/2019Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E-26/201.025/2021Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E-26/201.450/2022Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E-26/204.180/2024Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E26/210.410/2022Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E-26/211.289/2021Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E-26/211.378/2021Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro E-26/211.462/2019Instituto Nacional de Ciência e Tecnologia de Neurociência Translacional 465346/2014-6
6 · The paper itselfAbstract
Ischemic damage to the retina during development can lead to irreversible neuronal loss, driven in part by excitotoxic mechanisms and energy deprivation. While two-day caffeine exposure has previously been shown to confer neuroprotection in this context, it remained unclear whether acute administration during an ischemic event could yield similar benefits. In this study, we used an ex vivo model of oxygen and glucose deprivation (OGD) in chick embryo retinas to investigate whether a single, acute dose of caffeine applied during the insult reduces cell death and engages intracellular survival pathways. Results showed a significant reduction in OGD-induced cytotoxicity by caffeine exposure. However, unlike in the context of chronic exposure, acute caffeine exposure did not increase BDNF expression. Furthermore, antioxidant agents failed to mimic caffeine's protective effects, and acute caffeine exposure did not induce the expression of antioxidant response genes, nor oxidative stress or VEGF expression, suggesting that oxidative stress mitigation is not the primary mechanism for this effect. However, pharmacological antagonism of adenosine A
Indexed as
CaffeineIschemiaNeuroprotective AgentsRetinaAnimalsAntioxidantsCell DeathChick EmbryoGlucoseOxidative StressOxygenAntioxidantsCaffeineGlucoseNeuroprotective AgentsOxygenA2A receptorExcitotoxicityNeuroprotectionOxygen and glucose deprivation
Identifiers
PMID42129961
PMCPMC13399045
What Socratic holds
Textmetadata
LicenceCC BY
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