Evidence map›Paper›PMID 35835968›Full record

ReviewCellular and molecular neurobiology2023

Role of Pyroptosis, a Pro-inflammatory Programmed Cell Death, in Epilepsy.

Rabi Atabaki, Hossein Khaleghzadeh-Ahangar, Nardana Esmaeili, Parvaneh Mohseni-Moghaddam

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. PANoptosis in diabetes: immunometabolic insights and treatments.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. PANoptosis: A novel therapeutic target in kidney disease (Review).International journal of molecular medicine · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Ferroptosis and Pyroptosis in Epilepsy.Molecular neurobiology · 2024
    Review
  18. Article
  19. Review
  20. 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 at 4 institutions in 2 countries.

Rabi AtabakiRayan Research Center for Neuroscience & Behavior, Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran.
Hossein Khaleghzadeh-AhangarDepartment of Physiology, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Nardana EsmaeiliDepartment of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Parvaneh Mohseni-MoghaddamDepartment of Physiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. p.mohseni@iautmu.ac.ir.ORCID http://orcid.org/0000-0002-0608-2305
Babol University of Medical Sciences · IRFerdowsi University of Mashhad · IRIslamic Azad University Medical Branch of Tehran · IRUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is one of the most common serious brain diseases worldwide. Programmed cell death (PCD), a cellular self-destruction phenomenon, has been greatly documented in neurodegenerative diseases. Pyroptosis is a well-known pro-inflammatory PCD, and its involvement in epilepsy has been reported in animal models of epilepsy and also epileptic patients. Canonical (caspase-1-dependent) and non-canonical (caspase-1-independent) pathways are two main mechanisms implicated in pyroptotic cell death. Mouse caspase-11 or human analogues caspase-4/5 induce the non-canonical pathway. In both pathways, membrane gasdermin (GSDMD) pores contribute to pro-inflammatory cytokine release and lead to membrane destabilization and cell lysis. IL-1β and IL-18 are pro-inflammatory cytokines that are released following pyroptotic PCD. Brain inflammation increases excitability in the nervous system, promotes seizure activity, and is probably associated with the molecular and synaptic changes involved in epileptogenesis. Pro-inflammatory cytokines affect the glutamate and GABA neurotransmitter release as well as their receptors, thereby resulting in seizure activity. This review is intended to provide an overview of the current published works on pyroptotic cell death in epilepsy. The mechanisms by which pro-inflammatory cytokines, including IL-1β and IL-18 can promote epileptic discharges were also collected. According to this survey, since the involvement of pyroptosis in the development of epilepsy has been established, pyroptosis-targeted therapies may represent a novel anti-epileptogenic strategy.

Indexed as

EpilepsyPyroptosisAnimalsApoptosisCaspasesCytokinesHumansInflammasomesInterleukin-18MiceSeizuresCaspasesCytokinesInflammasomesInterleukin-18EpilepsyInflammationProgrammed cell deathPyroptosisSeizureStatus epilepticus

Identifiers

PMID35835968
PMCPMC11414441
OpenAlexW4285386170

What OpenQuestion 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 OpenQuestion graph.