Evidence map›Paper›PMID 31926631›Full record

ArticleRedox biology2020

Vitamin C controls neuronal necroptosis under oxidative stress.

Luciano Ferrada, María Jose Barahona, Katterine Salazar, Peter Vandenabeele, Francisco Nualart

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
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  6. Daily intake of antioxidants ameliorates PMFrontiers in nutrition · 2026
    Article
  7. Review
  8. Article
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  11. Review
  12. Review
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  15. Article
  16. Role of vitamin C and SVCT2 in neurogenesis.Frontiers in neuroscience · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Review
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

5 authors at 2 institutions in 2 countries.

Luciano FerradaLaboratory of Neurobiology and Stem Cells NeuroCellT, Department of Cellular Biology, Faculty of Biological Sciences, University of Concepcion, Concepcion, Chile; Center for Advanced Microscopy CMA BIO BIO, University of Concepcion, Concepcion, Chile.
María Jose BarahonaCenter for Advanced Microscopy CMA BIO BIO, University of Concepcion, Concepcion, Chile.
Katterine SalazarLaboratory of Neurobiology and Stem Cells NeuroCellT, Department of Cellular Biology, Faculty of Biological Sciences, University of Concepcion, Concepcion, Chile; Center for Advanced Microscopy CMA BIO BIO, University of Concepcion, Concepcion, Chile.
Peter VandenabeeleMolecular Signaling and Cell Death Unit, VIB Inflammation Research Center, Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
Francisco NualartLaboratory of Neurobiology and Stem Cells NeuroCellT, Department of Cellular Biology, Faculty of Biological Sciences, University of Concepcion, Concepcion, Chile; Center for Advanced Microscopy CMA BIO BIO, University of Concepcion, Concepcion, Chile. Electronic address: frnualart@udec.cl.
University of Concepción · CLGhent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Under physiological conditions, vitamin C is the main antioxidant found in the central nervous system and is found in two states: reduced as ascorbic acid (AA) and oxidized as dehydroascorbic acid (DHA). However, under pathophysiological conditions, AA is oxidized to DHA. The oxidation of AA and subsequent production of DHA in neurons are associated with a decrease in GSH concentrations, alterations in glucose metabolism and neuronal death. To date, the endogenous molecules that act as intrinsic regulators of neuronal necroptosis under conditions of oxidative stress are unknown. Here, we show that treatment with AA regulates the expression of pro- and antiapoptotic genes. Vitamin C also regulates the expression of RIPK1/MLKL, whereas the oxidation of AA in neurons induces morphological alterations consistent with necroptosis and MLKL activation. The activation of necroptosis by AA oxidation in neurons results in bubble formation, loss of membrane integrity, and ultimately, cellular explosion. These data suggest that necroptosis is a target for cell death induced by vitamin C.

Indexed as

Ascorbic AcidNecroptosisDehydroascorbic AcidNeuronsOxidation-ReductionOxidative StressAscorbic AcidDehydroascorbic AcidAscorbic acidDehydroascorbic acidLive cell microscopyNecroptosisNeuronal deathVitamin C

Identifiers

PMID31926631
PMCPMC6938857
OpenAlexW2994754289

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.