Evidence map›Paper›PMID 32391806›Full record

ReviewThe Journal of clinical investigation2020

Immune responses to stroke: mechanisms, modulation, and therapeutic potential.

Costantino Iadecola, Marion S Buckwalter, Josef Anrather

2 registry-linked trialsOpen access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 510 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
510citing papers in PubMed, 1 pooled it
35.5field-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.

NCT05512910 phase4active not recruitingnot on this mapstarted 2023, after this paper: background citation

Minocycline for Acute Ischemic Stroke Undergoing Endovascular Treatment Due to Basilar Artery Occlusion: a Randomized, Open-label, Proof of Concept Study

TypeinterventionalSponsorXijing HospitalRan2023 to 2025Enrolled90ConditionsIschemic Stroke, Acute, Minocycline, Endovascular Treatment, Basilar Artery OcclusionArmsMinocycline
NCT06077305 not yet recruitingnot on this mapstarted 2023, after this paper: background citation

A Registry Study of Microcirculation Disorder After Cerebral Small Vessel Disease and Ischemic Stroke, MODEST, Research Protocol

TypeobservationalSponsorBeijing Tiantan HospitalRan2023 to 2026Enrolled20,000ConditionsCerebral Small Vessel Diseases, Ischemic Stroke
3 · Its place in the literature

Who cites it

510 citing papers in PubMed, 1 synthesis or guideline pooled it, 787 citations in OpenAlex.

  1. Pooled it
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  14. Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026
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450 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 2 institutions in 1 country.

Costantino IadecolaFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York, USA.
Marion S BuckwalterDepartment of Neurology and Neurological Sciences, Stanford University Medical Center, Stanford, California, USA.
Josef AnratherFeil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York, USA.
Cornell University · USStanford Medicine · US

Funding

NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGER01NS034179 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IADECOLA, COSTANTINO · 1995 to 2021
$5.5M
Protective monocytes in cerebral ischemic toleranceR01NS081179 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI ANRATHER, JOSEF · 2012 to 2022
$3.7M
Immunomodulation by Commensal Microbiota: Role in Ischemic Brain InjuryR01NS094507 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI ANRATHER, JOSEF · 2016 to 2020
$1.9M
NINDS NIH HHS R01 NS034179NINDS NIH HHS R01 NS081179NINDS NIH HHS R01 NS094507
6 · The paper itself

Abstract

Stroke is the second leading cause of death worldwide and a leading cause of disability. Most strokes are caused by occlusion of a major cerebral artery, and substantial advances have been made in elucidating how ischemia damages the brain. In particular, increasing evidence points to a double-edged role of the immune system in stroke pathophysiology. In the acute phase, innate immune cells invade brain and meninges and contribute to ischemic damage, but may also be protective. At the same time, danger signals released into the circulation by damaged brain cells lead to activation of systemic immunity, followed by profound immunodepression that promotes life-threatening infections. In the chronic phase, antigen presentation initiates an adaptive immune response targeted to the brain, which may underlie neuropsychiatric sequelae, a considerable cause of poststroke morbidity. Here, we briefly review these pathogenic processes and assess the potential therapeutic value of targeting immunity in human stroke.

Indexed as

Adaptive ImmunityBrain IschemiaStrokeAnimalsHumansInflammation

Identifiers

PMID32391806
PMCPMC7260029
OpenAlexW3022448963

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.