Evidence map›Paper›PMID 25822341›Full record

ArticleCell death and differentiation2015

Activation of sirtuin 1 as therapy for the peroxisomal disease adrenoleukodystrophy.

L Morató, M Ruiz, J Boada, N Y Calingasan, J Galino, C Guilera, M Jové, A Naudí, I Ferrer, R Pamplona and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

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  14. Redox interplay between mitochondria and peroxisomes.Frontiers in cell and developmental biology · 2015
    Review
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

15 authors at 7 institutions in 2 countries.

L MoratóNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
M RuizNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
J BoadaExperimental Medicine Department, University of Lleida-IRBLleida, 25008 Lleida, Spain.
N Y CalingasanDepartment of Neurology and Neuroscience, Weill Cornell Medical College, 1006 New York, USA.
J GalinoNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
C GuileraNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
M JovéExperimental Medicine Department, University of Lleida-IRBLleida, 25008 Lleida, Spain.
A NaudíExperimental Medicine Department, University of Lleida-IRBLleida, 25008 Lleida, Spain.
I FerrerInstitute of Neuropathology, University of Barcelona, L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
R PamplonaExperimental Medicine Department, University of Lleida-IRBLleida, 25008 Lleida, Spain.
M SerranoTumor Suppression Group, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
M Portero-OtínExperimental Medicine Department, University of Lleida-IRBLleida, 25008 Lleida, Spain.
M F BealDepartment of Neurology and Neuroscience, Weill Cornell Medical College, 1006 New York, USA.
S FourcadeNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
A PujolNeurometabolic Diseases Laboratory, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
Biomedical Research Institute of Lleida · ESCentre for Biomedical Network Research on Rare Diseases · ESInstitut d'Investigació Biomédica de Bellvitge · ESCornell University · USSpanish National Cancer Research Centre · ESUniversitat de Barcelona · ESUniversitat de Lleida · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and mitochondrial failure are prominent factors in the axonal degeneration process. In this study, we demonstrate that sirtuin 1 (SIRT1), a key regulator of the mitochondrial function, is impaired in the axonopathy and peroxisomal disease X-linked adrenoleukodystrophy (X-ALD). We have restored SIRT1 activity using a dual strategy of resveratrol treatment or by the moderate transgenic overexpression of SIRT1 in a X-ALD mouse model. Both strategies normalized redox homeostasis, mitochondrial respiration, bioenergetic failure, axonal degeneration and associated locomotor disabilities in the X-ALD mice. These results indicate that the reactivation of SIRT1 may be a valuable strategy to treat X-ALD and other axonopathies in which the control of redox and energetic homeostasis is impaired.

Indexed as

AdrenoleukodystrophyAnimalsBlotting, WesternDisease Models, AnimalHumansIn Vitro TechniquesLocomotionMiceMice, Mutant StrainsOxidation-ReductionReal-Time Polymerase Chain ReactionResveratrolSirtuin 1StilbenesResveratrolSirtuin 1Stilbenes

Identifiers

PMID25822341
PMCPMC4648322
OpenAlexW2042672259

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.