Evidence map›Paper›PMID 33501625›Full record

ReviewMolecular neurobiology2021

Emerging Role of Microglia-Mediated Neuroinflammation in Epilepsy after Subarachnoid Hemorrhage.

Jun Wang, Jingxue Liang, Jiahong Deng, Xiaolin Liang, Kewan Wang, Hongxiao Wang, Dadi Qian, Hao Long, Kaijun Yang, Songtao Qi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Jun WangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. smuwangjun@163.com.ORCID http://orcid.org/0000-0003-3509-0790
Jingxue Liang *The First Clinical Medicine College, Southern Medical University, Guangzhou, China.
Jiahong Deng *The First Clinical Medicine College, Southern Medical University, Guangzhou, China.
Xiaolin Liang *The First Clinical Medicine College, Southern Medical University, Guangzhou, China.
Kewan WangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Hongxiao WangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Dadi QianDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Hao LongDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Kaijun YangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Songtao QiDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Nanfang Hospital · CNSouthern Medical University · CN

Funding

"Climbing Program" Special Fund of Guangdong Province pdjh2019b0100, pdjh2020b0112Natural Science Fund of Guangdong Province 2017A030313597Southern Medical University LX2016N006, KJ20161102, 201912121004S, 201912121013, S202012121088, X202012121354,19NJ-YB03
6 · The paper itself

Abstract

Epilepsy is a common and serious complication of subarachnoid hemorrhage (SAH), giving rise to increased morbidity and mortality. It's difficult to identify patients at high risk of epilepsy and the application of anti-epileptic drugs (AEDs) following SAH is a controversial topic. Therefore, it's pressingly needed to gain a better understanding of the risk factors, underlying mechanisms and the optimization of therapeutic strategies for epilepsy after SAH. Neuroinflammation, characterized by microglial activation and the release of inflammatory cytokines, has drawn growing attention due to its influence on patients with epilepsy after SAH. In this review, we discuss the risk factors for epilepsy after SAH and emphasize the critical role of microglia. Then we discuss how various molecules arising from pathophysiological changes after SAH activate specific receptors such as TLR4, NLRP3, RAGE, P2X7R and initiate the downstream inflammatory pathways. Additionally, we focus on the significant responses implicated in epilepsy including neuronal excitotoxicity, the disruption of blood-brain barrier (BBB) and the change of immune responses. As the application of AEDs for seizure prophylaxis after SAH remains controversial, the regulation of neuroinflammation targeting the key pathological molecules could be a promising therapeutic method. While neuroinflammation appears to contribute to epilepsy after SAH, more comprehensive experiments on their relationships are needed.

Indexed as

AnimalsBlood-Brain BarrierEpilepsyHumansInflammationMicrogliaRisk FactorsSubarachnoid HemorrhageEpilepsyMicrogliaNeuroinflammationSubarachnoid hemorrhage

Identifiers

PMID33501625
OpenAlexW3124365686

What Socratic holds

Textmetadata
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 Socratic graph.