Evidence map›Paper›PMID 18809468›Full record

ReviewNeuroscience2009

Toll-like receptor signaling in endogenous neuroprotection and stroke.

B J Marsh, R L Williams-Karnesky, M P Stenzel-Poore

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

135 citing papers in PubMed, 253 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Plasma NOTCH3 and the risk of cardiovascular recurrence in patients with ischemic stroke.QJM : monthly journal of the Association of Physicians · 2024
    Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Microglia: Key Players in Retinal Ageing and Neurodegeneration.Frontiers in cellular neuroscience · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Influence of the gut microbiome on inflammatory and immune response after stroke.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Review

75 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

3 authors at 1 institution in 1 country.

B J MarshDepartment of Molecular Microbiology and Immunology L220, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239, USA. marshb@ohsu.edu
R L Williams-Karnesky
M P Stenzel-Poore
Oregon Health & Science University · US

Funding

New Gene Expression in Cell Culture Models of IschemiaP01NS035965 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENBERG, DAVID ALAN · 1997 to 2007
$9.4M
Molecular Mechanisms of LPS Preconditioning In StrokeR01NS050567 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI STENZEL-POORE, MARY P · 2005 to 2015
$3.3M
Blood genomics and proteomics of CpG-induced neuroprotection in primate stroke.F30NS070359 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI WILLIAMS, REBECCA LYNN · 2010 to 2014
$220k
NINDS NIH HHS 5R01 NS050567NINDS NIH HHS F30 NS070359NINDS NIH HHS P01 NS035965NINDS NIH HHS R01 NS050567
6 · The paper itself

Abstract

Stroke and other cerebral vascular diseases are a leading cause of morbidity and mortality in the United States. Despite intensive research to identify interventions that lessen cerebrovascular injury, no major therapies exist. Development of stroke prophylaxis involves an understanding of the mechanisms of damage following cerebral ischemia, and elucidation of the endogenous mechanisms that combat further brain injury. Toll-like receptors (TLRs) are critical components of the innate immune system that have been shown recently to mediate ischemic injury. Paradoxically, TLR ligands administered systemically induce a state of tolerance to subsequent ischemic injury. Herein we suggest that stimulation of TLRs prior to ischemia reprograms TLR signaling that occurs following ischemic injury. Such reprogramming leads to suppressed expression of pro-inflammatory molecules and enhanced expression of numerous anti-inflammatory mediators that collectively confer robust neuroprotection. Our findings indicate that numerous preconditioning stimuli lead to TLR activation, an event that occurs prior to ischemia and ultimately leads to TLR reprogramming. Thus genomic reprogramming of TLR signaling may be a unifying principle of tolerance to cerebral ischemia.

Indexed as

AnimalsBrain InfarctionBrain IschemiaCytoprotectionEncephalitisGene Expression RegulationHumansImmune ToleranceNerve DegenerationSignal TransductionToll-Like ReceptorsToll-Like Receptors

Identifiers

PMID18809468
PMCPMC2674023
OpenAlexW2029784552

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.