Evidence map›Paper›PMID 39042218›Full record

ReviewMolecular neurobiology2025

Targeting NLRP3 Inflammasomes: A Trojan Horse Strategy for Intervention in Neurological Disorders.

Mohammad Amin Bayat Tork, Soroush Fotouhi, Parvin Roozi, Sajad Sahab Negah

Abstract readReview
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In one paragraph

Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
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.

Mohammad Amin Bayat TorkClinical Research Development Unit, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran.
Soroush FotouhiStudent Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran.
Parvin RooziDepartment of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Sajad Sahab NegahClinical Research Development Unit, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran. Sahabnegahs@mums.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, a growing focus has been on identifying critical mechanisms in neurological diseases that trigger a cascade of events, making it easier to target them effectively. One such mechanism is the inflammasome, an essential component of the immune response system that plays a crucial role in disease progression. The NLRP3 (nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain containing 3) inflammasome is a subcellular multiprotein complex that is widely expressed in the central nervous system (CNS) and can be activated by a variety of external and internal stimuli. When activated, the NLRP3 inflammasome triggers the production of proinflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18) and facilitates rapid cell death by assembling the inflammasome. These cytokines initiate inflammatory responses through various downstream signaling pathways, leading to damage to neurons. Therefore, the NLRP3 inflammasome is considered a significant contributor to the development of neuroinflammation. To counter the damage caused by NLRP3 inflammasome activation, researchers have investigated various interventions such as small molecules, antibodies, and cellular and gene therapy to regulate inflammasome activity. For instance, recent studies indicate that substances like micro-RNAs (e.g., miR-29c and mR-190) and drugs such as melatonin can reduce neuronal damage and suppress neuroinflammation through NLRP3. Furthermore, the transplantation of bone marrow mesenchymal stem cells resulted in a significant reduction in the levels of pyroptosis-related proteins NLRP3, caspase-1, IL-1β, and IL-18. However, it would benefit future research to have an in-depth review of the pharmacological and biological interventions targeting inflammasome activity. Therefore, our review of current evidence demonstrates that targeting NLRP3 inflammasomes could be a pivotal approach for intervention in neurological disorders.

Indexed as

InflammasomesMolecular Targeted TherapyNervous System DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsHumansInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinBiological interventionInflammasomeNeuroinflammationNeurological disordersNLRP3PyroptosisStem cell therapy

Identifiers

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.