Evidence map›Paper›PMID 32899616›Full record

ReviewInternational journal of molecular sciences2020

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches.

Carlo Domenico Maida, Rosario Luca Norrito, Mario Daidone, Antonino Tuttolomondo, Antonio Pinto

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 290 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
290citing papers in PubMed, 4 pooled it
31.5field-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.

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

290 citing papers in PubMed, 4 syntheses or guidelines pooled it, 597 citations in OpenAlex.

  1. Pooled it
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  10. Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026
    Article
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  16. NFAT1Cellular & molecular biology letters · 2026
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230 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

5 authors at 1 institution in 1 country.

Carlo Domenico MaidaU.O.C di Medicina Interna con Stroke Care, Dipartimento di Promozione della Salute, Materno-Infantile, di Medicina Interna e Specialistica di Eccellenza "G. D'Alessandro", University of Palermo, 90127 Palermo, Italy.ORCID 0000-0002-4868-9033
Rosario Luca NorritoU.O.C di Medicina Interna con Stroke Care, Dipartimento di Promozione della Salute, Materno-Infantile, di Medicina Interna e Specialistica di Eccellenza "G. D'Alessandro", University of Palermo, 90127 Palermo, Italy.
Mario DaidoneU.O.C di Medicina Interna con Stroke Care, Dipartimento di Promozione della Salute, Materno-Infantile, di Medicina Interna e Specialistica di Eccellenza "G. D'Alessandro", University of Palermo, 90127 Palermo, Italy.
Antonino TuttolomondoU.O.C di Medicina Interna con Stroke Care, Dipartimento di Promozione della Salute, Materno-Infantile, di Medicina Interna e Specialistica di Eccellenza "G. D'Alessandro", University of Palermo, 90127 Palermo, Italy.
Antonio PintoU.O.C di Medicina Interna con Stroke Care, Dipartimento di Promozione della Salute, Materno-Infantile, di Medicina Interna e Specialistica di Eccellenza "G. D'Alessandro", University of Palermo, 90127 Palermo, Italy.
University of Palermo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the most important causes of neurological morbidity and mortality in the world is ischemic stroke. It can be a result of multiple events such as embolism with a cardiac origin, occlusion of small vessels in the brain, and atherosclerosis affecting the cerebral circulation. Increasing evidence shows the intricate function played by the immune system in the pathophysiological variations that take place after cerebral ischemic injury. Following the ischemic cerebral harm, we can observe consequent neuroinflammation that causes additional damage provoking the death of the cells; on the other hand, it also plays a beneficial role in stimulating remedial action. Immune mediators are the origin of signals with a proinflammatory position that can boost the cells in the brain and promote the penetration of numerous inflammatory cytotypes (various subtypes of T cells, monocytes/macrophages, neutrophils, and different inflammatory cells) within the area affected by ischemia; this process is responsible for further ischemic damage of the brain. This inflammatory process seems to involve both the cerebral tissue and the whole organism in cardioembolic stroke, the stroke subtype that is associated with more severe brain damage and a consequent worse outcome (more disability, higher mortality). In this review, the authors want to present an overview of the present learning of the mechanisms of inflammation that takes place in the cerebral tissue and the role of the immune system involved in ischemic stroke, focusing on cardioembolic stroke and its potential treatment strategies.

Indexed as

AnimalsBrainBrain IschemiaCytokinesEmbolic StrokeHumansInflammationIschemic StrokeNeuroimmunomodulationStrokeCytokinescardiac embolismischemic strokeneuroinflammation

Identifiers

PMID32899616
PMCPMC7555650
OpenAlexW3083125992

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.