Evidence map›Paper›PMID 36035987›Full record

ReviewFrontiers in cell and developmental biology2022

Crosstalk between neuroinflammation and oxidative stress in epilepsy.

Timothy Fabisiak, Manisha Patel

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 3 pooled it
14.2field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 3 syntheses or guidelines pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

16 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Timothy FabisiakDepartment of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Center, Aurora, CO, United States.
Manisha PatelDepartment of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Center, Aurora, CO, United States.
University of Montana · US

Funding

SUPEROXIDE RADICALS IN SEIZURE-INDUCED NEURONAL DEATHR01NS039587 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2000 to 2019
$5.9M
Redox Control of Seizure-Induced Neuroinflammation.R01NS086423 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2013 to 2022
$3.0M
Mitochondrial Mechanisms of Astrogliosis in EpilesyR37NS039587 · NINDS · UNIVERSITY OF COLORADO DENVER · PI MANISHA N PATEL · 2022 to 2026
$2.8M
Mitochondrial mechanisms of redox cycling agentsR01NS045748 · NINDS · UNIVERSITY OF COLORADO DENVER · PI PATEL, MANISHA N · 2004 to 2013
$2.6M
NINDS NIH HHS R01 NS039587NINDS NIH HHS R01 NS045748NINDS NIH HHS R01 NS086423NINDS NIH HHS R37 NS039587
6 · The paper itself

Abstract

The roles of both neuroinflammation and oxidative stress in the pathophysiology of epilepsy have begun to receive considerable attention in recent years. However, these concepts are predominantly studied as separate entities despite the evidence that neuroinflammatory and redox-based signaling cascades have significant crosstalk. Oxidative post-translational modifications have been demonstrated to directly influence the function of key neuroinflammatory mediators. Neuroinflammation can further be controlled on the transcriptional level as the transcriptional regulators NF-KB and nrf2 are activated by reactive oxygen species. Further, neuroinflammation can induce the increased expression and activity of NADPH oxidase, leading to a highly oxidative environment. These factors additionally influence mitochondria function and the metabolic status of neurons and glia, which are already metabolically stressed in epilepsy. Given the implication of this relationship to disease pathology, this review explores the numerous mechanisms by which neuroinflammation and oxidative stress influence one another in the context of epilepsy. We further examine the efficacy of treatments targeting oxidative stress and redox regulation in animal and human epilepsies in the literature that warrant further investigation. Treatment approaches aimed at rectifying oxidative stress and aberrant redox signaling may enable control of neuroinflammation and improve patient outcomes.

Indexed as

epilepsymitochondriaNADPH oxidaseneuroinflammationoxidative stressredox

Identifiers

PMID36035987
PMCPMC9399352
OpenAlexW4292449016

What Socratic holds

Textmetadata
LicenceCC BY
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.