Evidence map›Paper›PMID 36799538›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023

Biomimetic Remodeling of Microglial Riboflavin Metabolism Ameliorates Cognitive Impairment by Modulating Neuroinflammation.

Mengran Zhang, Huaqing Chen, Wenlong Zhang, Yan Liu, Liuyan Ding, Junwei Gong, Runfang Ma, Shaohui Zheng, Yunlong Zhang

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
9.2field-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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
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  5. Expanding roles of cGAS-STING signaling in neuroinflammation.The Journal of clinical investigation · 2026
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  18. Cell type-specific master metabolic regulators of Alzheimer's disease.bioRxiv : the preprint server for biology · 2025
    Article
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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 at 4 institutions in 1 country.

Mengran ZhangDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Huaqing ChenShenzhen Key Laboratory of Gene and Antibody Therapy, Center for Biotechnology and Biomedicine, State Key Laboratory of Chemical Oncogenomics, State Key Laboratory of Health Sciences and Technology, Institute of Biopharmaceutical and Health Engineering, Shenzhen International Graduate School, Tsinghua University, Shenzhen, Guangdong, 518055, China.
Wenlong ZhangDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Yan LiuSchool of Traditional Chinese Medicine, Jinan University, Guangzhou, 510632, China.
Liuyan DingDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Junwei GongDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Runfang MaDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Shaohui ZhengDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Yunlong ZhangDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.ORCID 0000-0002-2447-9138
Second Affiliated Hospital of Guangzhou Medical University · CNFirst Affiliated Hospital of Guangzhou Medical University · CNShandong University of Traditional Chinese Medicine · CNShenzhen University Health Science Center · CN

Funding

China Postdoctoral Science Foundation 2021M700951Fundamental Research Funds for the Central Universities 21621002Guangzhou Medical University Discipline Construction Funds JCXKJS2022A09National Natural Science Foundation of China 82101325National Natural Science Foundation of China 82104416National Natural Science Foundation of China 82174468Project of Administration of Traditional Chinese Medicine of Guangdong Province of China 20221101Science and Technology Planning Project of Guangzhou 201904010238
6 · The paper itself

Abstract

Neuroinflammation, for which microglia are the predominant contributors, is a significant risk factor for cognitive dysfunction. Riboflavin (also known as vitamin B2) ameliorates cognitive impairment via anti-oxidative stress and anti-inflammation properties; however, the underlying mechanisms linking riboflavin metabolism and microglial function in cognitive impairment remain unclear. Here, it is demonstrated that riboflavin kinase (RFK), a critical enzyme in riboflavin metabolism, is specifically expressed in microglia. An intermediate product of riboflavin, flavin mononucleotide (FMN), inhibited RFK expression via regulation of lysine-specific methyltransferase 2B (KMT2B). FMN supplementation attenuated the pro-inflammatory TNFR1/NF-κB signaling pathway, and this effect is abolished by KMT2B overexpression. To improve the limited anti-inflammatory efficiency of free FMN, a biomimetic microglial nanoparticle strategy (designated as MNPs@FMN) is established, which penetrated the blood brain barrier with enhanced microglial-targeted delivery efficiency. Notably, MNPs@FMN ameliorated cognitive impairment and dysfunctional synaptic plasticity in a lipopolysaccharide-induced inflammatory mouse model and in a 5xFAD mouse model of Alzheimer's disease. Taken together, biomimetic microglial delivery of FMN may serve as a potential therapeutic approach for inflammation-dependent cognitive decline.

Indexed as

Cognitive DysfunctionMicrogliaAnimalsBiomimeticsMiceNeuroinflammatory DiseasesRiboflavinRiboflavincognitive declineflavin mononucleotidemicroglial targeted deliveryNeuroinflammationriboflavin kinase

Identifiers

PMID36799538
PMCPMC10131853
OpenAlexW4321168396

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.