Evidence map›Paper›PMID 23504609›Full record

ReviewTranslational stroke research2013

Steps to translate preconditioning from basic research to the clinic.

Frances R Bahjat, Raffaella Gesuete, Mary P Stenzel-Poore

Abstract readReview
In one paragraph

Review in Translational stroke research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Vascular neural network in subarachnoid hemorrhage.Translational stroke research · 2014
    Article
  13. Effects of catalpol on ATPase and amino acids in gerbils with cerebral ischemia/reperfusion injury.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014
    Article
  14. Review
  15. Article
  16. Article
  17. Article
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.

Frances R BahjatDepartment of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon.
Raffaella Gesuete
Mary P Stenzel-Poore

Funding

NINDS Cooperative Program in Translational ResearchU01NS064953 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI STENZEL-POORE, MARY P · 2009 to 2014
$8.2M
Ultrastructure and Single Particle Microscopy CoreP30NS061800 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI AICHER, SUE A · 2009 to 2020
$6.6M
Molecular Mechanisms of LPS Preconditioning In StrokeR01NS050567 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI STENZEL-POORE, MARY P · 2005 to 2015
$3.3M
Toll-like Receptors: Novel targets of neuroprotection in ischemic brain injuryR01NS062381 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI STENZEL-POORE, MARY P · 2009 to 2013
$1.8M
NINDS NIH HHS P30 NS061800NINDS NIH HHS R01 NS050567NINDS NIH HHS R01 NS062381NINDS NIH HHS U01 NS064953
6 · The paper itself

Abstract

Efforts to treat cardiovascular and cerebrovascular diseases often focus on the mitigation of ischemia-reperfusion (I/R) injury. Many treatments or "preconditioners" are known to provide substantial protection against the I/R injury when administered prior to the event. Brief periods of ischemia itself have been validated as a means to achieve neuroprotection in many experimental disease settings, in multiple organ systems, and in multiple species suggesting a common pathway leading to tolerance. In addition, pharmacological agents that act as potent preconditioners have been described. Experimental induction of neuroprotection using these various preconditioning paradigms has provided a unique window into the brain's endogenous protective mechanisms. Moreover, preconditioning agents themselves hold significant promise as clinical-stage therapies for prevention of I/R injury. The aim of this article is to explore several key steps involved in the preclinical validation of preconditioning agents prior to the conduct of clinical studies in humans. Drug development is difficult, expensive and relies on multi-factorial analysis of data from diverse disciplines. Importantly, there is no single path for the preclinical development of a novel therapeutic and no proven strategy to ensure success in clinical translation. Rather, the conduct of a diverse array of robust preclinical studies reduces the risk of clinical failure by varying degrees depending upon the relevance of preclinical models and drug pharmacology to humans. A strong sense of urgency and high tolerance of failure are often required to achieve success in the development of novel treatment paradigms for complex human conditions.

Indexed as

Ischemic PreconditioningTranslational Research, BiomedicalAnimalsBlood-Brain BarrierBrain IschemiaDisease Models, AnimalDrug Evaluation, PreclinicalHumansMiceNeuroprotective AgentsRatsNeuroprotective Agentsanimal models of strokebrain injurycardiovascular diseasecerebral ischemiaischemiaischemic brain injuryMCAOmousenonhuman primateocclusionPreconditioningrepercussionstroketherapeutictoll-like receptors

Identifiers

PMID23504609
PMCPMC3595131

What OpenQuestion holds

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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.