Evidence map›Paper›PMID 26392570›Full record

ArticleEMBO reports2015

Resistance of glia-like central and peripheral neural stem cells to genetically induced mitochondrial dysfunction--differential effects on neurogenesis.

Blanca Díaz-Castro, Ricardo Pardal, Paula García-Flores, Verónica Sobrino, Rocío Durán, José I Piruat, José López-Barneo

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  6. Maternal Inflammation During Pregnancy and Offspring Brain Development: The Role of Mitochondria.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2022
    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

7 authors at 3 institutions in 1 country.

Blanca Díaz-CastroInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain.
Ricardo PardalInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain Departamento de Fisiología Médica y Biofísica, Universidad de Sevilla, Sevilla, Spain Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
Paula García-FloresInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
Verónica SobrinoInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain.
Rocío DuránInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain.
José I PiruatInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain lbarneo@us.es jpiruat-ibis@us.es.
José López-BarneoInstituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain Departamento de Fisiología Médica y Biofísica, Universidad de Sevilla, Sevilla, Spain Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain lbarneo@us.es jpiruat-ibis@us.es.
Universidad de Sevilla · ESInstituto de Biomedicina de Sevilla · ESHospital Universitario Virgen del Rocío · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria play a central role in stem cell homeostasis. Reversible switching between aerobic and anaerobic metabolism is critical for stem cell quiescence, multipotency, and differentiation, as well as for cell reprogramming. However, the effect of mitochondrial dysfunction on neural stem cell (NSC) function is unstudied. We have generated an animal model with homozygous deletion of the succinate dehydrogenase subunit D gene restricted to cells of glial fibrillary acidic protein lineage (hGFAP-SDHD mouse). Genetic mitochondrial damage did not alter the generation, maintenance, or multipotency of glia-like central NSCs. However, differentiation to neurons and oligodendrocytes (but not to astrocytes) was impaired and, hence, hGFAP-SDHD mice showed extensive brain atrophy. Peripheral neuronal populations were normal in hGFAP-SDHD mice, thus highlighting their non-glial (non hGFAP(+)) lineage. An exception to this was the carotid body, an arterial chemoreceptor organ atrophied in hGFAP-SDHD mice. The carotid body contains glia-like adult stem cells, which, as for brain NSCs, are resistant to genetic mitochondrial damage.

Indexed as

NeurogenesisAnimalsAstrocytesBrainCarotid BodyDisease Models, AnimalGene DeletionGlial Fibrillary Acidic ProteinMiceMitochondriaNeural Stem CellsNeurogliaNeuronsOligodendrogliaSuccinate DehydrogenaseGlial Fibrillary Acidic ProteinSuccinate Dehydrogenasecarotid body stem cellsmitochondrial dysfunctionneural stem cellsperipheral versus central neurogenesis

Identifiers

PMID26392570
PMCPMC4641503
OpenAlexW2152770326

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.