Evidence map›Paper›PMID 30965198›Full record

ArticleRedox biology2019

Neuroprotective effects of EpoL against oxidative stress induced by soluble oligomers of Aβ peptide.

C Castillo, C Fernández-Mendívil, I Buendia, P Saavedra, C Meza, N C Parra, M G Lopez, J R Toledo, J Fuentealba

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Oxidative Stress in Brain Function.Antioxidants (Basel, Switzerland) · 2025
    Review
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  9. MicroalgaeFrontiers in cell and developmental biology · 2020
    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

9 authors at 2 institutions in 2 countries.

C CastilloLaboratorio de Biotecnología y Biofarmacos, Departamento de Fisiopatologia, Facultad de Ciencias Biológicas, Universidad de Concepcion, Chile.
C Fernández-MendívilDepartamento de Farmacología y Terapéutica, Instituto Teófilo Hernando, Universidad Autónoma de Madrid, Spain.
I BuendiaDepartamento de Farmacología y Terapéutica, Instituto Teófilo Hernando, Universidad Autónoma de Madrid, Spain.
P SaavedraLaboratorio de Biotecnología y Biofarmacos, Departamento de Fisiopatologia, Facultad de Ciencias Biológicas, Universidad de Concepcion, Chile.
C MezaLaboratorio de Biotecnología y Biofarmacos, Departamento de Fisiopatologia, Facultad de Ciencias Biológicas, Universidad de Concepcion, Chile.
N C ParraLaboratorio de Biotecnología y Biofarmacos, Departamento de Fisiopatologia, Facultad de Ciencias Biológicas, Universidad de Concepcion, Chile.
M G LopezDepartamento de Farmacología y Terapéutica, Instituto Teófilo Hernando, Universidad Autónoma de Madrid, Spain.
J R ToledoLaboratorio de Biotecnología y Biofarmacos, Departamento de Fisiopatologia, Facultad de Ciencias Biológicas, Universidad de Concepcion, Chile. Electronic address: jotoledo@udec.cl.
J FuentealbaLaboratorio de Screening de Compuestos Neuroactivos, Departamento de Fisiología, Facultad de Ciencias Biológicas, Universidad de Concepcion, Chile; Centro de Investigaciones Avanzadas en Biomedicina (CIAB-UdeC), Facultad de Ciencias Biológicas, Universidad de Concepcion, Chile. Electronic address: jorgefuentealba@udec.cl.
University of Concepción · CLUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erythropoietin is a glycoproteic hormone that regulates hematopoiesis by acting on its specific receptor (EpoR). The expression of EpoR in the central nervous system (CNS) suggests a role for this hormone in the brain. Recently, we developed a new Epo variant without hematopoietic activity called EpoL, which showed marked neuroprotective effects against oxidative stress in brain ischemia related models. In this study, we have evaluated the neuroprotective effects of EpoL against oxidative stress induced by chronic treatment with Aβ. Our results show that EpoL was neuroprotective against Aβ-induced toxicity by a mechanism that implicates EpoR, reduction in reactive oxygen species, and reduction in astrogliosis. Furthermore, EpoL treatment improved calcium handling and SV2 levels. Interestingly, the neuroprotective effect of EpoL against oxidative stress induced by chronic Aβ treatment was achieved at a concentration 10 times lower than that of Epo. In conclusion, EpoL, a new variant of Epo without hematopoietic activity, is of potential interest for the treatment of diseases related to oxidative stress in the CNS such as Alzheimer disease.

Indexed as

Amyloid beta-PeptidesAnimalsCalcium SignalingCell Line, TumorCell SurvivalErythropoietinGoatsMilkNeuroprotective AgentsOxidative StressPeptide FragmentsProtein MultimerizationReactive Oxygen SpeciesReceptors, ErythropoietinRecombinant ProteinsAmyloid beta-PeptidesErythropoietinNeuroprotective AgentsPeptide FragmentsReactive Oxygen SpeciesReceptors, ErythropoietinRecombinant ProteinsAlzheimer diseaseAmyloid betaErythropoietinGlycosylationNeuroprotectionOxidative stress

Identifiers

PMID30965198
PMCPMC6454060
OpenAlexW2934917816

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.