Evidence map›Paper›PMID 23547115›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Overexpression of SIRT1 protein in neurons protects against experimental autoimmune encephalomyelitis through activation of multiple SIRT1 targets.

Vamshi K Nimmagadda, Christopher T Bever, Narasimha R Vattikunta, Saifi Talat, Vakas Ahmad, Naveen K Nagalla, David Trisler, Susan I V Judge, Walter Royal, Krish Chandrasekaran and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Pooled it
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  14. Article
  15. Cell-Specific Expression of Human SIRT1 by Gene Therapy Reduces Retinal Ganglion Cell Loss Induced by Elevated Intraocular Pressure.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  16. Article
  17. Downregulation of SF3B2 protects CNS neurons in models of multiple sclerosis.Annals of clinical and translational neurology · 2023
    Article
  18. Evaluation of Rosuvastatin Therapy onCurrent therapeutic research, clinical and experimental · 2023
    Article
  19. Review
  20. Review

8 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 1 country.

Vamshi K NimmagaddaVeterans Affairs Maryland Healthcare System, Baltimore, MD 21201, USA.
Christopher T Bever
Narasimha R Vattikunta
Saifi Talat
Vakas Ahmad
Naveen K Nagalla
David Trisler
Susan I V Judge
Walter Royal
Krish Chandrasekaran
James W Russell
Tapas K Makar
University of Maryland, Baltimore · USMultiple Sclerosis Center of Atlanta · USVA Maryland Health Care System · US

Funding

SIRT1 Overexpression in Cellular Mitochondrial Metabolism and FunctionR21RR024888 · NCRR · UNIVERSITY OF MARYLAND BALTIMORE · PI RUSSELL, JAMES W · 2008 to 2009
$413k
NCRR NIH HHS R21 RR024888NCRR NIH HHS RR024888
6 · The paper itself

Abstract

Treatment of experimental autoimmune encephalomyelitis (EAE) with resveratrol, an activator of sirtuin 1 (SIRT1), reduces disease severity. This suggested that activators of SIRT1, a highly conserved NAD-dependent protein deacetylase, might have immune-modulating or neuroprotective therapeutic effects in EAE. Previously, we showed that SIRT1 expression increases in EAE, suggesting that it is an adaptive response. In this study, we investigated the potential function of SIRT1 in regulating EAE using SIRT1-overexpressing mice. The current studies examine potential neuroprotective and immunomodulatory effects of SIRT1 overexpression in chronic EAE induced by immunization of C57BL/6 mice with myelin oligodendrocyte glycoprotein peptide 35-55. SIRT1 suppressed EAE clinical symptoms compared with wild-type EAE mice and prevented or altered the phenotype of inflammation in spinal cords; as a result, demyelination and axonal injury were reduced. Significant neuroprotective effects were observed, with fewer apoptotic cells found in the spinal cords of SIRT1-overexpressing EAE mice associated with increased brain-derived neurotrophic factor and NAD levels. Earlier, we showed that brain-derived neurotrophic factor and NAD play crucial neuroprotective roles in EAE. These results suggest that SIRT1 reduces neuronal loss in this chronic demyelinating disease model and that this is associated with a reduction in inflammation.

Indexed as

AnimalsApoptosisAxonsBrain-Derived Neurotrophic FactorDemyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalFemaleInflammationMiceMice, Inbred C57BLMyelin-Oligodendrocyte GlycoproteinNADNeuronsNeuroprotective AgentsResveratrolSirtuin 1Brain-Derived Neurotrophic FactorMyelin-Oligodendrocyte GlycoproteinNADNeuroprotective AgentsResveratrolSirt1 protein, mouseSirtuin 1Stilbenes

Identifiers

PMID23547115
PMCPMC3963275
OpenAlexW2167933097

What OpenQuestion holds

Textmetadata
LicenceTDM
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.