Evidence map›Paper›PMID 40501216›Full record

ArticleScience progress

HMGB1 mediates inflammation response of epileptogenicity in tuberous sclerosis complex-related epilepsy.

Suhui Kuang, Tinghong Liu, Liu Yuan, Jinshan Xu, Yangshuo Wang, Feng Chen, Shuli Liang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science progress. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Immune dysregulation and epileptogenesis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
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

7 authors.

Suhui KuangFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, China.ORCID 0009-0005-1945-3450
Tinghong LiuFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, China.ORCID 0000-0003-0156-7490
Liu YuanFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, China.ORCID 0009-0007-3932-5610
Jinshan XuFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, China.ORCID 0009-0006-5078-8301
Yangshuo WangFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-4172-6081
Feng ChenFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, China.ORCID 0000-0001-7410-0926
Shuli LiangFunctional Neurosurgery Department, National Children's Health Center of China, Beijing Children's Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-7292-745X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ObjectiveEpileptogenic tubers (ETs) contribute to the epileptogenesis in patients with tuberous sclerosis complex (TSC). High mobility group protein B-1 (HMGB1) triggers inflammatory responses that impact neuronal electrical activity. We aimed to study the role of HMGB1 in epileptogenicity in TSC-related epilepsy.MethodsThis study included both human and animal models. ETs were identified through comprehensive preoperative evaluations and postoperative seizure outcomes following tuberectomy. Immunofluorescence was performed to assess the positive area and fluorescence intensity of HMGB1 and IL-1β in ETs and non-ETs. TSC2-GFAP-CKO mice and epileptic models were established. Mice in the prevention group (postnatal day 14) received daily injections of monoclonal HMGB1 or IL-1β antibodies for 22 days. Mice in the intervention group (postnatal day 28) received identical treatments. Genetic and proteomic analyses of HMGB1 and IL-1β were conducted on both TSC patients and animal models.ResultsHMGB1 and IL-1β were significantly overexpressed in ETs compared to non-ETs. HMGB1 was predominantly nuclear in non-ETs but mainly cytoplasmic in ETs. In animal models, HMGB1 and IL-1β expression at both the gene and protein levels was significantly upregulated in the TSC2-deficient group compared to the wild-type group. IL-1β expression was lower in the HMGB1-intervention group than in the model control group. Seizure frequency was reduced in both HMGB1 and IL-1β prevention and intervention groups compared to the model control.ConclusionsThe interference of HMGB1 and IL-1β significantly reduced the frequency of seizure attacks in TSC. Epileptic seizures serve as key triggers for HMGB1 translocation and subsequent release into the cytoplasm, contributing to seizure recurrence.

Indexed as

EpilepsyHMGB1 ProteinInflammationTuberous SclerosisAnimalsChildDisease Models, AnimalFemaleHumansInterleukin-1betaMaleMiceMice, KnockoutTuberous Sclerosis Complex 2 ProteinHMGB1 ProteinHMGB1 protein, humanHMGB1 protein, mouseInterleukin-1betaTuberous Sclerosis Complex 2 ProteinEpilepsyepileptogenicityhigh mobility group protein b-1 (HMGB1)interleukin 1β (IL-1β)tuberous sclerosis complex

Identifiers

PMID40501216
PMCPMC12163276

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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.