Evidence map›Paper›PMID 29434374›Full record

ArticleNature cell biology2018

Reactive oxygen species regulate axonal regeneration through the release of exosomal NADPH oxidase 2 complexes into injured axons.

Arnau Hervera, Francesco De Virgiliis, Ilaria Palmisano, Luming Zhou, Elena Tantardini, Guiping Kong, Thomas Hutson, Matt C Danzi, Rotem Ben-Tov Perry, Celio X C Santos and 9 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Nature cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 190 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 1 pooled it
13.8field-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

190 citing papers in PubMed, 1 synthesis or guideline pooled it, 326 citations in OpenAlex.

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  5. Exercise Training Stimulates the Release of Glutathione Peroxidase 1 (GPX1)-Enriched Extracellular Vesicles That Promote Angiogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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130 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 8 institutions in 5 countries.

Arnau HerveraMolecular Neuroregeneration, Division of Brain Sciences, Department of Medicine, Imperial College London, London, UK.
Francesco De VirgiliisMolecular Neuroregeneration, Division of Brain Sciences, Department of Medicine, Imperial College London, London, UK.
Ilaria PalmisanoMolecular Neuroregeneration, Division of Brain Sciences, Department of Medicine, Imperial College London, London, UK.
Luming ZhouLaboratory for NeuroRegeneration and Repair, Center for Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Elena TantardiniMolecular Neuroregeneration, Division of Brain Sciences, Department of Medicine, Imperial College London, London, UK.
Guiping KongLaboratory for NeuroRegeneration and Repair, Center for Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Thomas HutsonMolecular Neuroregeneration, Division of Brain Sciences, Department of Medicine, Imperial College London, London, UK.
Matt C DanziThe Miami Project to Cure Paralysis, Department of Neurological Surgery, Miller School of Medicine, University of Miami, Miami, FL, USA.
Rotem Ben-Tov PerryDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.
Celio X C SantosCardiovascular Division, British Heart Foundation Centre of Research Excellence, King's College London, London, UK.
Alexander N KapustinCardiovascular Division, British Heart Foundation Centre of Research Excellence, King's College London, London, UK.
Roland A FleckCentre for Ultrastructural Imaging, King's College London, London, UK.
José Antonio Del RíoCellular and Molecular Neurobiotechnology, Institute for Bioengineering of Catalonia, Barcelona, Spain.ORCID http://orcid.org/0000-0002-5214-4909
Thomas CarrollBioinformatics Resource Centre, The Rockefeller University, New York, NY, USA.
Vance LemmonThe Miami Project to Cure Paralysis, Department of Neurological Surgery, Miller School of Medicine, University of Miami, Miami, FL, USA.
John L BixbyThe Miami Project to Cure Paralysis, Department of Neurological Surgery, Miller School of Medicine, University of Miami, Miami, FL, USA.
Ajay M ShahCardiovascular Division, British Heart Foundation Centre of Research Excellence, King's College London, London, UK.
Mike FainzilberDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0001-8173-8557
Simone Di GiovanniMolecular Neuroregeneration, Division of Brain Sciences, Department of Medicine, Imperial College London, London, UK. s.di-giovanni@imperial.ac.uk.ORCID http://orcid.org/0000-0003-3154-5399
Hertie Institute for Clinical Brain Research · DEKing's College London · GBImperial College London · GBUniversity of Miami · USWeizmann Institute of Science · ILBiomedical Research Networking Center on Neurodegenerative Diseases · ESInstitute for Bioengineering of Catalonia · ESRockefeller University · US

Funding

Novel Gene Targets for CNS Axonal RegenerationR01HD057632 · NICHD · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BIXBY, JOHN L, LEMMON, VANCE P · 2007 to 2018
$4.7M
British Heart Foundation PG/16/70/32310British Heart Foundation RG/13/11/30384
6 · The paper itself

Abstract

Reactive oxygen species (ROS) contribute to tissue damage and remodelling mediated by the inflammatory response after injury. Here we show that ROS, which promote axonal dieback and degeneration after injury, are also required for axonal regeneration and functional recovery after spinal injury. We find that ROS production in the injured sciatic nerve and dorsal root ganglia requires CX3CR1-dependent recruitment of inflammatory cells. Next, exosomes containing functional NADPH oxidase 2 complexes are released from macrophages and incorporated into injured axons via endocytosis. Once in axonal endosomes, active NOX2 is retrogradely transported to the cell body through an importin-β1-dynein-dependent mechanism. Endosomal NOX2 oxidizes PTEN, which leads to its inactivation, thus stimulating PI3K-phosporylated (p-)Akt signalling and regenerative outgrowth. Challenging the view that ROS are exclusively involved in nerve degeneration, we propose a previously unrecognized role of ROS in mammalian axonal regeneration through a NOX2-PI3K-p-Akt signalling pathway.

Indexed as

Nerve DegenerationNerve RegenerationAnimalsAxonsbeta KaryopherinsCell LineCX3C Chemokine Receptor 1Disease Models, AnimalDyneinsEndocytosisEndosomesExosomesGanglia, SpinalMacrophagesMice, Inbred C57BLMice, Knockoutbeta KaryopherinsCX3C Chemokine Receptor 1Cx3cr1 protein, mouseCybb protein, mouseDyneinsKpnb1 protein, mouseNADPH Oxidase 2Nuclear ProteinsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseReactive Oxygen Species

Identifiers

PMID29434374
OpenAlexW2793768313

What OpenQuestion holds

Textmetadata
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.