ReviewNaunyn-Schmiedeberg's archives of pharmacology2025
Mitochondrial dysfunction and NLRP3 inflammasome activation in drug-resistant epilepsy: emerging insights and mitochondrial-targeted therapeutic strategies.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Neuroinflammation in Epilepsy: Biochemical and Molecular Mechanisms and Implications for Natural Product-Driven Drug Discovery.International journal of molecular sciences · 2026Review
- Article
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug-resistant epilepsy (DRE) is a substantial medical challenge due to the scarcity of effective therapies. Newly identified mechanisms, such as mitochondrial dysfunction and the Nod-like receptor protein (NLRP3) inflammasome activation, are implicated in playing an important role in the pathogenesis of DRE. Mitochondria are crucial for maintaining neuronal energy balance and cell viability. The NLRP3 inflammasome is triggered when mitochondria are damaged, releasing reactive oxygen species (ROS) and mitochondrial DNA. This activation leads to a cascade of pro-inflammatory reactions, exacerbating neuronal damage and seizures. This review highlights the proposed molecular mechanism involving the interplay of mitochondrial impairment with precipitated NLRP3 inflammasome activation in DRE. It also explores the possibility of implementing drug-delivery techniques to deliver antiseizure medications (ASMs) with agents reversing mitochondrial damage as a novel approach to treat DRE. These advanced delivery methods might improve the efficacy of ASMs, aid in overcoming drug resistance observed in epilepsy, and thus offer a promising means of ameliorating seizure activity in DRE.
Indexed as
Identifiers
40699241What OpenQuestion holds
Registered trials
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.