Evidence map›Paper›PMID 40500710›Full record

ArticleJournal of nanobiotechnology2025

Coordination acid-engineered Prussian Blue affects glycometabolic reprogramming in microglia for epileptic treatment.

Yao Zhao, Feixiang Chen, Chen Chen, Yuling Yang, Luo Wang, Jiaqi Zhu, Xin Wang, Yanyan Liu, Jing Ding

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Antiepileptic and antiepileptogenic effects ofIBRO neuroscience reports · 2026
    Article
  2. 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

9 authors.

Yao Zhao *Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Feixiang Chen *Department of Materials Science and State Key Laboratory of Molecular Engineering of Polymers, Academy for Engineering and Technology, Fudan University, Shanghai, 200433, China.
Chen Chen *Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Yuling YangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Luo WangDepartment of Materials Science and State Key Laboratory of Molecular Engineering of Polymers, Academy for Engineering and Technology, Fudan University, Shanghai, 200433, China.
Jiaqi ZhuDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Xin WangDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. wang.xin@zs-hospital.sh.cn.
Yanyan LiuDepartment of Materials Science and State Key Laboratory of Molecular Engineering of Polymers, Academy for Engineering and Technology, Fudan University, Shanghai, 200433, China. liuyyan@fudan.edu.cn.
Jing DingDepartment of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. ding.jing@zs-hospital.sh.cn.

Funding

National Funds for General Projects 52272269National Funds for General Projects 82271499Natural Science Foundation of China Youth Fund 52322213
6 · The paper itself

Abstract

Seizures induce significant immune and metabolic stress in microglia, but the interaction between these processes remains unclear. This study, utilizing single-nucleus RNA sequencing data from temporal lobe epilepsy (TLE) patients, reveals that reactive oxygen species (ROS) stabilize hypoxia-inducible factor 1-alpha (HIF-1α), thereby inducing glycometabolic reprogramming in microglia and driving the development of a pro-inflammatory phenotype. To address this, a coordination acid-engineered Prussian Blue (PB@ZIF) nanosystem is developed, where Zn²⁺ sites in the zeolitic imidazolate framework (ZIF) lower the local pKa, thereby enhancing the reaction efficiency of PB with free radicals. In vivo experiments using a TLE model demonstrate that PB@ZIF is effectively internalized by microglia and significantly alleviates spontaneous recurrent seizures and seizure-related behaviors. PB@ZIF mitigates microglial inflammatory activation and reduces neuronal injury. Notably, PB@ZIF-induced ROS reduction enhances the enzymatic activity of prolyl hydroxylase domain enzymes, effectively inhibiting HIF-1α-driven glycometabolic reprogramming in microglia. This study identifies a molecular mechanism underlying the immune-metabolic interactions in epilepsy and proposes a promising therapeutic strategy regulating microglial metabolism to improve epilepsy management.

Indexed as

EpilepsyEpilepsy, Temporal LobeFerrocyanidesMicrogliaAnimalsHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMiceReactive Oxygen SpeciesZeolitesferric ferrocyanideFerrocyanidesHypoxia-Inducible Factor 1, alpha SubunitReactive Oxygen SpeciesZeolitesLocal pKaMetabolic reprogrammingMicrogliaNanocatalystTemporal lobe epilepsy

Identifiers

PMID40500710
PMCPMC12153168

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.