Evidence map›Paper›PMID 34489498›Full record

ArticleScientific reports2021

HSPA9/Mortalin mediates axo-protection and modulates mitochondrial dynamics in neurons.

Cécile A Ferré, Anne Thouard, Alexandre Bétourné, Anne-Louise Le Dorze, Pascale Belenguer, Marie-Christine Miquel, Jean-Michel Peyrin, Daniel Gonzalez-Dunia, Marion Szelechowski

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

18 citing papers in PubMed, 19 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Cécile A Ferré *Toulouse Institute for Infectious and Inflamatory Diseases (Infinity), Université Toulouse, CNRS, Inserm, UPS, Toulouse, France.
Anne Thouard *Toulouse Institute for Infectious and Inflamatory Diseases (Infinity), Université Toulouse, CNRS, Inserm, UPS, Toulouse, France.
Alexandre BétournéToulouse Institute for Infectious and Inflamatory Diseases (Infinity), Université Toulouse, CNRS, Inserm, UPS, Toulouse, France.
Anne-Louise Le DorzeToulouse Institute for Infectious and Inflamatory Diseases (Infinity), Université Toulouse, CNRS, Inserm, UPS, Toulouse, France.
Pascale BelenguerCentre de Recherches sur la Cognition Animale (CRCA), Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.
Marie-Christine MiquelCentre de Recherches sur la Cognition Animale (CRCA), Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.
Jean-Michel PeyrinSorbonne Universités, Faculté des Sciences et Technologie, CNRS UMR 8246, INSERM U1130, Neurosciences Paris Seine, Institut de Biologie Paris Seine, Paris, France.
Daniel Gonzalez-DuniaToulouse Institute for Infectious and Inflamatory Diseases (Infinity), Université Toulouse, CNRS, Inserm, UPS, Toulouse, France. daniel.dunia@inserm.fr.
Marion SzelechowskiToulouse Institute for Infectious and Inflamatory Diseases (Infinity), Université Toulouse, CNRS, Inserm, UPS, Toulouse, France. marion.szelechowski@inserm.fr.
Inserm · FRUniversité Fédérale de Toulouse Midi-Pyrénées · FRCentre National de la Recherche Scientifique · FRCentre de Recherches sur la Cognition Animale · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mortalin is a mitochondrial chaperone protein involved in quality control of proteins imported into the mitochondrial matrix, which was recently described as a sensor of neuronal stress. Mortalin is down-regulated in neurons of patients with neurodegenerative diseases and levels of Mortalin expression are correlated with neuronal fate in animal models of Alzheimer's disease or cerebral ischemia. To date, however, the links between Mortalin levels, its impact on mitochondrial function and morphology and, ultimately, the initiation of neurodegeneration, are still unclear. In the present study, we used lentiviral vectors to over- or under-express Mortalin in primary neuronal cultures. We first analyzed the early events of neurodegeneration in the axonal compartment, using oriented neuronal cultures grown in microfluidic-based devices. We observed that Mortalin down-regulation induced mitochondrial fragmentation and axonal damage, whereas its over-expression conferred protection against axonal degeneration mediated by rotenone exposure. We next demonstrated that Mortalin levels modulated mitochondrial morphology by acting on DRP1 phosphorylation, thereby further illustrating the crucial implication of mitochondrial dynamics on neuronal fate in degenerative diseases.

Indexed as

AnimalsCerebral CortexHSP70 Heat-Shock ProteinsMitochondrial DynamicsNeuronsRatsRats, Sprague-DawleyRotenoneHSP70 Heat-Shock ProteinsmortalinRotenone

Identifiers

PMID34489498
PMCPMC8421332
OpenAlexW3114616269

What OpenQuestion holds

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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.