Evidence map›Paper›PMID 40211861›Full record

ArticleClinical and experimental pediatrics2025

NLRP3 inflammasome: a key player in neonatal brain injury.

Cagla Kiser, Ilkcan Ercan, Defne Engur, Sermin Genc

Abstract read
In one paragraph

Article in Clinical and experimental pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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

4 authors.

Cagla KiserIzmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Izmir, Turkey.
Ilkcan ErcanIzmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Izmir, Turkey.
Defne EngurDepartment of Neonatology, Izmir Faculty of Medicine, University of Health Sciences, Izmir, Turkey.
Sermin GencIzmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Izmir, Turkey.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among neonates, hypoxic-ischemic encephalopathy is the most significant cause of mortality and hypoxia-ischemia is among the leading causes of brain damage. The microglia are primary mediators of neuroinflammation. NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation is the first line of defense in the central nervous system. Numerous studies have shown that the NLRP3 inflammasome is activated and proinflammatory cytokines are upregulated upon hypoxia-ischemia-induced brain damage. However, aberrant activation of the NLRP3 inflammasome results in cell death and brain tissue damage. Given that neonates are particularly vulnerable to neuroinflammation, which may cause lifelong disabilities, it is important to target the pathways involved in its complex nature to improve their prognosis. The potential use of compounds or drugs that target inflammasome activation to relieve hypoxia-induced brain damage has become significant. This review describes the NLRP3 inflammasome in neonates to contribute to the development of therapeutic approaches.

Indexed as

Brain injuryHypoxiaNeonatalNLRP3 inflammasome

Identifiers

PMID40211861
PMCPMC12235344

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.