Evidence map›Paper›PMID 22030546›Full record

ArticleNature neuroscience2011

Stroke research at a crossroad: asking the brain for directions.

Costantino Iadecola, Josef Anrather

Registry-linked trialAbstract read
In one paragraph

Article in Nature neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03448159 (FLOW Trial), which is not on this map. Cited by 216 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 4 pooled it
–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.

NCT03448159 phase2completednot on this mapstarted 2019, after this paper: background citation

FLOW Trial: Fluoxetine to Open the Critical Period Time Window to Improve Motor Recovery After Stroke

TypeinterventionalSponsorUniversity Health Network, TorontoRan2019 to 2022Enrolled52ConditionsStroke, Cerebrovascular Accident, Cerebral Infarction, Brain InfarctionArmsFluoxetine Hydrochloride, Placebo, Exercise Program
3 · Its place in the literature

Who cites it

216 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Albumin therapy for acute ischemic stroke: a meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Pooled it
  4. Pooled it
  5. The effect of repeated remote ischemic postconditioning after an ischemic stroke (REPOST): A randomized controlled trial.International journal of stroke : official journal of the International Stroke Society · 2023
    Trial
  6. Trial
  7. A prospective test of the late effects of potentially antineuroplastic drugs in a stroke rehabilitation study.International journal of stroke : official journal of the International Stroke Society · 2014
    Trial
  8. Trial
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

156 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

2 authors.

Costantino IadecolaDivision of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York, USA. coi2001@med.cornell.edu
Josef Anrather

Funding

Role of COX-2 Gene Expression in Ischemic Brain DamageR01NS035806 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 1997 to 2010
$3.5M
NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGER37NS034179 · NINDS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 1999 to 2005
$1.8M
NINDS NIH HHS NS35806NINDS NIH HHS R01 NS035806NINDS NIH HHS R37 NS034179NINDS NIH HHS R37-NS34179
6 · The paper itself

Abstract

Ischemic stroke remains a vexing public health problem. Although progress has been made in prevention and supportive care, efforts to protect the brain from ischemic cell death have failed. Thus, no new treatment has made it from bench to bedside since tissue plasminogen activator was introduced in 1996. The brain has a remarkable capacity for self-preservation, illustrated by the protective responses induced by ischemia, preconditioning and exercise. Here we describe the mechanisms underlying brain self-protection, with the goal of identifying features that could provide insight into stroke therapy. Unlike traditional therapeutic approaches based on counteracting selected pathways of the ischemic cascade, endogenous neuroprotection relies on coordinated neurovascular programs that support cerebral perfusion, mitigate the harmful effects of cerebral ischemia and promote tissue restoration. Learning how the brain triggers and implements these protective measures may advance our quest to treat stroke.

Indexed as

AnimalsBrainExerciseHumansModels, BiologicalNeuroprotective AgentsStrokeNeuroprotective Agents

Identifiers

PMID22030546
PMCPMC3633153

What OpenQuestion holds

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Registered trials

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.