Evidence map›Paper›PMID 26938300›Full record

ArticleCell death & disease2016

Knockout of Atg5 delays the maturation and reduces the survival of adult-generated neurons in the hippocampus.

Y Xi, J S Dhaliwal, M Ceizar, M Vaculik, K L Kumar, D C Lagace

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 87 citations in OpenAlex.

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  8. Heavy metal-induced disruption of the autophagy-lysosomal pathway: implications for aging and neurodegenerative disorders.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
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  14. Serum autophagy-related gene 5 level in stroke patients: correlation with CD4+ T cells and cognition impairment during a 3-year follow-up.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
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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

6 authors at 1 institution in 1 country.

Y XiDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa K1H 8M5, Ontario, Canada.
J S DhaliwalDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa K1H 8M5, Ontario, Canada.
M CeizarDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa K1H 8M5, Ontario, Canada.
M VaculikDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa K1H 8M5, Ontario, Canada.
K L KumarDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa K1H 8M5, Ontario, Canada.
D C LagaceDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa K1H 8M5, Ontario, Canada.
University of Ottawa · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved lysosomal degradation pathway that plays important roles in cell maintenance, expansion and differentiation. Removal of genes essential for autophagy from embryonic neural stem and precursor cells reduces the survival and inhibits neuronal differentiation of adult-generated neurons. No study has modified autophagy within the adult precursor cells, leaving the cell-autonomous role of autophagy in adult neurogenesis unknown. Here we demonstrate that autophagic flux exists in the adult dividing progenitor cells and their progeny in the dentate gyrus. To investigate the role of autophagy in adult hippocampal neurogenesis, we genetically deleted Autophagy-related gene 5 (Atg5) that reduced autophagic flux and the survival of the progeny of dividing progenitor cells. This significant reduction in survival of adult-generated neurons is accompanied by a delay in neuronal maturation, including a transient reduction in spine density in the absence of a change in differentiation. The delay in cell maturation and loss of progeny of the Atg5-null cells was not present in mice that lacked the essential pro-apoptotic protein Bax (Bcl-2-associated X protein), suggesting that Atg5-deficient cells die through a Bax-dependent mechanism. In addition, there was a loss of Atg5-null cells following exposure to running, suggesting that Atg5 is required for running-induced increases in neurogenesis. These findings highlight the cell-autonomous requirement of Atg5 in the survival of adult-generated neurons.

Indexed as

Adult Stem CellsAnimalsAutophagyAutophagy-Related Protein 5bcl-2-Associated X ProteinCell SurvivalGene Knockdown TechniquesHippocampusMiceMice, KnockoutMicrotubule-Associated ProteinsNeural Stem CellsNeurogenesisNeuronsAtg5 protein, mouseAutophagy-Related Protein 5Bax protein, mousebcl-2-Associated X ProteinMicrotubule-Associated Proteins

Identifiers

PMID26938300
PMCPMC4823925
OpenAlexW2292716261

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.