Evidence map›Paper›PMID 34526897›Full record

ReviewFrontiers in pharmacology2021

Targeting NLRP3 Inflammasome in Translational Treatment of Nervous System Diseases: An Update.

Qingying Yu, Tingting Zhao, Molin Liu, Duo Cao, Jiaxin Li, Yanling Li, Mengyao Xia, Xiaoyu Wang, Tingting Zheng, Chuanguo Liu and 2 more

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
–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

29 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  18. New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Review
  19. Article
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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

12 authors.

Qingying YuSchool of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.
Tingting ZhaoSchool of Foreign Languages, Shandong University of Traditional Chinese Medicine, Jinan, China.
Molin LiuSchool of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.
Duo CaoCollege of Life Science, Yan'an University, Yan'an, China.
Jiaxin LiSchool of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.
Yanling LiSchool of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.
Mengyao XiaSchool of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.
Xiaoyu WangSchool of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.
Tingting ZhengSchool of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.
Chuanguo LiuInnovation Research Institute of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.
Xiangyu MuSchool of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.
Peng SunInnovation Research Institute of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammatory response is the immune response mechanism of the innate immune system of the central nervous system. Both primary and secondary injury can activate neuroinflammatory response. Among them, the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome plays a key role in the inflammatory response of the central system. Inflammasome is a type of pattern recognition receptor, a cytoplasmic polyprotein complex composed of members of the Nod-like receptor (NLR) family and members of the pyrin and HIN domain (PYHIN) family, which can be affected by a variety of pathogen-related molecular patterns or damage-related molecular patterns are activated. As one of the research hotspots in the field of medical research in recent years, there are increasing researches on immune function abnormalities in the onset of neurological diseases such as depression, AD, ischemic brain injury and cerebral infarction, the NLRP3 inflammasome causes the activated caspase-1 to cleave pre-interleukin-1β and pre-interleukin-18 into mature interleukin-1β and interleukin-18, in turn, a large number of inflammatory factors are produced, which participate in the occurrence and development of the above-mentioned diseases. Targeted inhibition of the activation of inflammasomes can reduce the inflammatory response, promote the survival of nerve cells, and achieve neuroprotective effects. This article reviews NLRP3 inflammasome's role in neurological diseases and related regulatory mechanisms, which providing references for future research in this field.

Indexed as

Alzheimer’s diseasedepressioninflammasomeintracranial haemorrhageischemic strokenervous system diseaseNLRP3

Identifiers

PMID34526897
PMCPMC8435574

What OpenQuestion holds

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Registered trials

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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.