Evidence map›Paper›PMID 32152318›Full record

ArticleNature communications2020

Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin.

Debia Wakhloo, Franziska Scharkowski, Yasmina Curto, Umer Javed Butt, Vikas Bansal, Agnes A Steixner-Kumar, Liane Wüstefeld, Ashish Rajput, Sahab Arinrad, Matthias R Zillmann and 12 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
13.0field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 155 citations in OpenAlex.

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  11. Increased plasma levels of erythropoietin after renal denervation in patients with resistant hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
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  16. Nobiletin: a potential erythropoietin receptor activator protects renal cells against hypoxia.Apoptosis : an international journal on programmed cell death · 2025
    Article
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22 more citing papers are in PubMed but not listed here.

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

22 authors at 5 institutions in 3 countries.

Debia Wakhloo *Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0003-3288-857X
Franziska Scharkowski *Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0001-9112-4444
Yasmina Curto *Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0001-8087-360X
Umer Javed ButtClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Vikas BansalClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0002-0944-7226
Agnes A Steixner-KumarClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0001-7913-2716
Liane WüstefeldClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Ashish RajputInstitute of Medical Systems Biology, Center for Molecular Neurobiology, University Clinic Hamburg-Eppendorf, Hamburg, Germany.ORCID http://orcid.org/0000-0002-6741-8861
Sahab ArinradClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0002-7083-1358
Matthias R ZillmannClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0002-4222-0947
Anna SeelbachClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0002-7908-7369
Imam HassounaClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Katharina SchneiderClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Abdul Qadir IbrahimInstitute of Medical Systems Biology, Center for Molecular Neurobiology, University Clinic Hamburg-Eppendorf, Hamburg, Germany.ORCID http://orcid.org/0000-0003-3452-8500
Hauke B WernerDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID http://orcid.org/0000-0002-7710-5738
Henrik MartensSynaptic Systems GmbH, Göttingen, Germany.ORCID http://orcid.org/0000-0002-5589-983X
Kamilla MiskowiakCopenhagen Affective Disorder Research Centre, Psychiatric Centre Copenhagen, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-2572-1384
Sonja M WojcikDepartment of Molecular Neurobiology, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Stefan BonnInstitute of Medical Systems Biology, Center for Molecular Neurobiology, University Clinic Hamburg-Eppendorf, Hamburg, Germany.
Juan NacherNeurobiology Unit, Program in Neurosciences and Interdisciplinary Research Structure for Biotechnology and Biomedicine (BIOTECMED), Universitat de València, Burjassot, Spain.
Klaus-Armin NaveDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany. nave@em.mpg.de.ORCID http://orcid.org/0000-0001-8724-9666
Hannelore EhrenreichClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany. ehrenreich@em.mpg.de.ORCID http://orcid.org/0000-0001-8371-5711
Max Planck Institute of Experimental Medicine · DEUniversität Hamburg · DENanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 · DEUniversitat de València · ESCopenhagen University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, improved performance on complex running wheels after EPO is imitated by exposure to mild exogenous/inspiratory hypoxia. All these effects depend on neuronal expression of the Epor gene. This suggests a model of neuroplasticity in form of a fundamental regulatory circle, in which neuronal networks-challenged by cognitive tasks-drift into transient hypoxia, thereby triggering neuronal EPO/EPOR expression.

Indexed as

NeurogenesisNeuronal PlasticityAnimalsBrainCell DifferentiationCognitionDendritic SpinesErythropoietinFemaleGene DeletionHumansHypoxiaMaleMice, Inbred C57BLModels, NeurologicalMotor ActivityErythropoietinProto-Oncogene Proteins c-fosReceptors, Erythropoietin

Identifiers

PMID32152318
PMCPMC7062779
OpenAlexW3009163926

What OpenQuestion holds

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LicenceCC BY
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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.