Evidence map›Paper›PMID 33050466›Full record

ArticleInternational journal of molecular sciences2020

Activation of STAT3 Regulates Reactive Astrogliosis and Neuronal Death Induced by AβO Neurotoxicity.

Danira Toral-Rios, Genaro Patiño-López, Gisela Gómez-Lira, Rafael Gutiérrez, Fernando Becerril-Pérez, Aldebarán Rosales-Córdova, Juan Carlos León-Contreras, Rogelio Hernández-Pando, Ismael León-Rivera, Isabel Soto-Cruz and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  5. Article
  6. Amyloid-Frontiers in neuroscience · 2026
    Review
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  8. Article
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  15. Article
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  18. Astrocytic EphA4 signaling is important for the elimination of excitatory synapses in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Review
  20. Article
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

12 authors at 8 institutions in 2 countries.

Danira Toral-RiosDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de Mexico 07360, Mexico.ORCID 0000-0001-5156-6969
Genaro Patiño-LópezLaboratorio de Investigación en Inmunología y Proteómica, Hospital Infantil de México Federico Gómez, Ciudad de Mexico 06720, Mexico.ORCID 0000-0002-8716-722X
Gisela Gómez-LiraDepartamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de Mexico 14330, Mexico.ORCID 0000-0001-7519-5664
Rafael GutiérrezDepartamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de Mexico 14330, Mexico.
Fernando Becerril-PérezResearch Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), Campus-Vienna-BioCenter 1, 1030 Vienna, Austria.
Aldebarán Rosales-CórdovaDepartamento de Administración, Facultad de Economía y Negocios, Universidad Anáhuac de México, Huixquilucan 52786, Mexico.
Juan Carlos León-ContrerasDepartamento de Patología, Sección Patología Experimental, Instituto Nacional de Ciencias Médicas y Nutrición, Salvador Zubirán, Ciudad de Mexico 14080, Mexico.ORCID 0000-0001-8827-1670
Rogelio Hernández-PandoDepartamento de Patología, Sección Patología Experimental, Instituto Nacional de Ciencias Médicas y Nutrición, Salvador Zubirán, Ciudad de Mexico 14080, Mexico.
Ismael León-RiveraCentro de Investigaciones Químicas, IICBA, Universidad Autónoma del Estado de Morelos, Cuernavaca Morelos 62210, Mexico.
Isabel Soto-CruzLaboratorio de Oncología Molecular, Facultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México, Ciudad de Mexico 09230, Mexico.ORCID 0000-0001-5115-3654
Benjamín Florán-GarduñoDepartamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de Mexico 07360, Mexico.ORCID 0000-0002-3430-9335
Victoria Campos-PeñaLaboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Ciudad de Mexico 14269, Mexico.ORCID 0000-0001-8282-7543
Instituto Politécnico Nacional · MXInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MXHospital Infantil de México Federico Gómez · MXInstituto Nacional de Neurología y Neurocirugía · MXResearch Institute of Molecular Pathology · ATUniversidad Anáhuac · MXUniversidad Autónoma del Estado de Morelos · MXUniversidad Nacional Autónoma de México · MX

Funding

CONACYT S0008-2016-1 Nº 273182
6 · The paper itself

Abstract

Amyloid-beta oligomers (AβO) have been proposed as the most potent neurotoxic and inflammation inducers in Alzheimer's disease (AD). AβO contribute to AD pathogenesis by impairing the production of several cytokines and inflammation-related signaling pathways, such as the Janus kinases/signal transducer of transcription factor-3 (JAK/STAT3) pathway. STAT3 modulates glial activation, indirectly regulates Aβ deposition, and induces cognitive decline in AD transgenic models. However, in vivo studies using an AβO microinjection rat model have not yet explored STAT3 role. The main purpose of this study was to elucidate if a single microinjection of AβO could promote an increased expression of STAT3 in glial cells favoring neuroinflammation and neurodegeneration. We designed a model of intrahippocampal microinjection and assessed glial activation, cytokines production, STAT3 expression, and neurodegeneration in time. Our results showed robust expression of STAT3 in glial cells (mainly in astrocytes) and neurons, correlating with neuronal death in response to AβO administration. A STAT3 inhibition assay conducted in rat primary hippocampal cultures, suggested that the induction of the transcription factor by AβO in astrocytes leads them to an activation state that may favor neuronal death. Notwithstanding, pharmacological inhibition of the JAK2/STAT3 pathway should be focused on astrocytes because it is also essential in neurons survival. Overall, these findings strongly suggest the participation of STAT3 in the development of neurodegeneration.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesBiomarkersCell DeathDisease Models, AnimalDisease SusceptibilityFluorescent Antibody TechniqueGliosisHippocampusImmunohistochemistryNeuronsProtein AggregatesProtein Aggregation, PathologicalProtein MultimerizationAmyloid beta-PeptidesBiomarkersProtein AggregatesSTAT3 Transcription FactorAlzheimer’s diseaseneuroinflammationneurotoxicityoligomersSTAT3β-amyloid

Identifiers

PMID33050466
PMCPMC7590075
OpenAlexW3092458823

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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.