Evidence map›Paper›PMID 26971449›Full record

ArticleNature communications2016

Promotion of mitochondrial biogenesis by necdin protects neurons against mitochondrial insults.

Koichi Hasegawa, Toru Yasuda, Chinatsu Shiraishi, Kazushiro Fujiwara, Serge Przedborski, Hideki Mochizuki, Kazuaki Yoshikawa

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 73 citations in OpenAlex.

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  13. Modeling neuromuscular diseases in zebrafish.Frontiers in molecular neuroscience · 2022
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  14. Necdin: A purposive integrator of molecular interaction networks for mammalian neuron vitality.Genes to cells : devoted to molecular & cellular mechanisms · 2021
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  18. Synergistic Effects of Milk-Derived Exosomes and Galactose onInternational journal of molecular sciences · 2021
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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 2 institutions in 2 countries.

Koichi HasegawaLaboratory of Regulation of Neuronal Development, Institute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan.
Toru YasudaDepartment of Neurology, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.
Chinatsu ShiraishiLaboratory of Regulation of Neuronal Development, Institute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan.
Kazushiro FujiwaraLaboratory of Regulation of Neuronal Development, Institute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan.
Serge PrzedborskiDepartment of Neurology, Pathology and Cell Biology, Columbia University, New York, New York, 10032, USA.
Hideki MochizukiDepartment of Neurology, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.ORCID http://orcid.org/0000-0002-0874-7542
Kazuaki YoshikawaLaboratory of Regulation of Neuronal Development, Institute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan.
The University of Osaka · JPColumbia University Irving Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurons rely heavily on mitochondria for their function and survival. Mitochondrial dysfunction contributes to the pathogenesis of neurodegenerative diseases such as Parkinson's disease. PGC-1α is a master regulator of mitochondrial biogenesis and function. Here we identify necdin as a potent PGC-1α stabilizer that promotes mitochondrial biogenesis via PGC-1α in mammalian neurons. Expression of genes encoding mitochondria-specific proteins decreases significantly in necdin-null cortical neurons, where mitochondrial function and expression of the PGC-1α protein are reduced. Necdin strongly stabilizes PGC-1α by inhibiting its ubiquitin-dependent degradation. Forced expression of necdin enhances mitochondrial function in primary cortical neurons and human SH-SY5Y neuroblastoma cells to prevent mitochondrial respiratory chain inhibitor-induced degeneration. Moreover, overexpression of necdin in the substantia nigra in vivo of adult mice protects dopaminergic neurons against degeneration in experimental Parkinson's disease. These data reveal that necdin promotes mitochondrial biogenesis through stabilization of endogenous PGC-1α to exert neuroprotection against mitochondrial insults.

Indexed as

Organelle BiogenesisAnimalsBlotting, WesternCerebral CortexDisease Models, AnimalDNA, MitochondrialDopaminergic NeuronsGene ExpressionHEK293 CellsHumansImmunohistochemistryImmunoprecipitationMembrane Potential, MitochondrialMiceMice, KnockoutMitochondriaDNA, MitochondrialMitochondrial ProteinsnecdinNerve Tissue ProteinsNuclear ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseTranscription Factors

Identifiers

PMID26971449
PMCPMC4793078
OpenAlexW2301440237

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.