Evidence map›Paper›PMID 30113480›Full record

ReviewMedicine2018

The role of NLRP3 inflammasome in stroke and central poststroke pain.

Shao-Jun Li, Yu-Fen Zhang, Se-Hui Ma, Yao Yi, Hong-Yan Yu, Lei Pei, Dan Feng

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. A hematoma location-based nomogram for individualized prediction of thalamic pain after spontaneous thalamic hemorrhage.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. The P2X7 Hypothesis of Central Post-Stroke Pain.International journal of molecular sciences · 2024
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. The effect and mechanism of exercise for post-stroke pain.Frontiers in molecular neuroscience · 2022
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Shao-Jun LiDepartment of Pain Management, Wuhan First Hospital Department of Neurobiology, School of Basic Medicine, Tongji Medical College The Institute for Brain Research (IBR), Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, Wuhan, China.
Yu-Fen Zhang
Se-Hui Ma
Yao Yi
Hong-Yan Yu
Lei Pei
Dan Feng
Huazhong University of Science and Technology · CNTongji University · CNWuhan Third Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNLRP3 inflammasome plays a prominent role in the pathogenesis and progression of many diseases, such as type 2 diabetes mellitus, obesity, atherosclerosis, and Alzheimer's disease. However, little knowledge is known about the role of NLRP3 inflammasome in central post-stroke pain (CPSP).

methodsWe selected relevant studies by searching PubMed, Embase, and Medline from inception through February, 2018. We systematically reviewed available publications according to the terms "NLRP3 inflammasome" and "stroke" or "central post-stroke pain" in the title/abstract field.

resultsWe reviewed the articles and put forward two possible ways for NLRP3 inflammasome in CPSP. One way is that NLRP3 activation causes cerebral cortex injure, decreasing descending projection fiber to thalamus. Such condition may let GABAergic releases reduce, making the ventral basal (VB) neurons excitability increased. Finally, CPSP occur. Another way is that NLRP3 inflammasome leads to thalamic lesion and strengthens inflammatory response of microglia at the same time. Persistent inflammation causes GABAergic alteration in thalamus reticular neurons (TRN) to restrain VB interneurons functions, contributing to CPSP.

conclusionsThese possible mechanisms will help become knowledgeable about the occurrence CPSP and provide potential therapy for CPSP.

Indexed as

Cerebral CortexHumansInflammasomesNeuralgiaNeuronsNLR Family, Pyrin Domain-Containing 3 ProteinPainStrokeThalamusInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID30113480
PMCPMC6112889
OpenAlexW2886181407

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.