Evidence map›Paper›PMID 31989468›Full record

ArticleNeurochemical research2021

Intertwined ROS and Metabolic Signaling at the Neuron-Astrocyte Interface.

Carlos Vicente-Gutiérrez, Daniel Jiménez-Blasco, Rubén Quintana-Cabrera

Abstract read
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In one paragraph

Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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  13. Pathophysiology of Lipid Droplets in Neuroglia.Antioxidants (Basel, Switzerland) · 2021
    Review
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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

3 authors.

Carlos Vicente-GutiérrezInstitute of Functional Biology and Genomics (IBFG), University of Salamanca, CSIC, Salamanca, Spain.ORCID http://orcid.org/0000-0002-6481-595X
Daniel Jiménez-BlascoInstitute of Functional Biology and Genomics (IBFG), University of Salamanca, CSIC, Salamanca, Spain.ORCID http://orcid.org/0000-0002-1384-1832
Rubén Quintana-CabreraInstitute of Functional Biology and Genomics (IBFG), University of Salamanca, CSIC, Salamanca, Spain. ruben310@usal.es.ORCID http://orcid.org/0000-0002-0601-349X

Funding

H2020 Marie Skłodowska-Curie Actions 793987
6 · The paper itself

Abstract

Metabolism and redox signalling share critical nodes in the nervous system. In the last years, a series of major findings have challenged the current vision on how neural reactive oxygen species (ROS) are produced and handled in the nervous system. Once regarded as deleterious by-products, ROS are now shown to be essential for a metabolic and redox crosstalk. In turn, this coupling defines neural viability and function to control behaviour or leading to neurodegeneration when compromised. Findings like a different assembly of mitochondrial respiratory supercomplexes in neurons and astrocytes stands behind a divergent production of ROS in either cell type, more prominent in astrocytes. ROS levels are however tightly controlled by an antioxidant machinery in astrocytes, assumed as more efficient than that of neurons, to regulate redox signalling. By exerting this control in ROS abundance, metabolic functions are finely tuned in both neural cells. Further, a higher engagement of mitochondrial respiration and oxidative function in neurons, underpinned by redox equivalents supplied from the pentose phosphate pathway and from glia, differs from the otherwise strong glycolytic capacity of astrocytes. Here, we recapitulate major findings on how ROS and metabolism differ between neural cells but merge to define reciprocal signalling pathways, ultimately defining neural function and fate.

Indexed as

AnimalsAstrocytesGlutathioneGlycolysisHumansLactic AcidMitochondriaNeuronsReactive Oxygen SpeciesSignal TransductionGlutathioneLactic AcidReactive Oxygen SpeciesAstrocyteMetabolismMitochondriaNeurodegenerationNeuronOxidative stress

Identifiers

What OpenQuestion holds

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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.