Evidence map›Paper›PMID 40581646›Full record

ArticleJournal of neuroinflammation2025

Genetically-engineered Salmonella typhimurium expressing FGF21 promotes neurological recovery in ischemic stroke via FGFR1/AMPK/mTOR pathway.

Dongchen Xu, Min Wen, Bingwa Lebohang Anesu, Xijun Chen, Yuhao Chen, Wenqi Qian, Chenguang Yang, Jin Hai Zheng, Yinan Zhou, Haoqi Ni and 3 more

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

13 authors.

Dongchen Xu *Zhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Min Wen *Department of Neurosurgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510000, China.
Bingwa Lebohang Anesu *Zhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Xijun ChenZhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Yuhao ChenInstitute of Hypoxia Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, 325035, China.
Wenqi QianZhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Chenguang YangZhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Jin Hai ZhengSchool of Biomedical Sciences, Hunan University, Changsha, 410082, China.
Yinan ZhouZhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Haoqi NiZhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Kunlin JinDepartment of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX, 76107, USA.
Qichuan ZhugeZhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. qc.zhuge@wmu.edu.cn.
Su YangZhejiang - US Joint Laboratory for Aging and Neurological Disease Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. yangsu@wmu.edu.cn.

Funding

National Natural Science Foundation of China 82171469National Natural Science Foundation of China U24A20697Natural Science Foundation of Zhejiang Province LQ22H090010Wenzhou Municipal Science and Technology Bureau Y20240105
6 · The paper itself

Abstract

backgroundIschemic stroke (IS) remains a leading cause of mortality and disability, with limited therapeutic options due to poor drug delivery to ischemic lesions. To address this challenge, an engineered Salmonella based therapeutic method for targeted drug delivery and long-term treatment is herein designed to mitigate ischemic damage.

methodsWe engineered an attenuated luminescent Salmonella typhimurium (S.t -ΔpG) strain with an L-arabinose-inducible pBAD system to secrete bioactive FGF21. C57BL/6 mice were used to to measure neuron apoptosis and the activity of immune cells following IS induction plus S.t-ΔpG injection. Bioluminescence imaging was applied for bacterial colonization. ELISA and glucose uptake assays were performed to detect FGF21 secretion and the bioactivity. Neurological tests, TTC staining, and TUNEL labeling were used to assess the therapeutic effects of barterially secreted FGF21. Immunofluorescence assay of FGF21/FGFR1 dominant pathway was explored to investigate neuroprotective mechanism, while IBA-1 staining, CD3/CD68 immunostaining, cytokine profiling, and hepatorenal histopathology were detected to evaluate biosecurity.

resultsS.t-ΔpG

conclusionOur study presents a novel, Salmonella - based platform for targeted and sustained FGF21 delivery, offering a promising therapeutic strategy for ischemic stroke with robust efficacy and minimal systemic toxicity.

Indexed as

Fibroblast Growth FactorsIschemic StrokeRecovery of FunctionSalmonella typhimuriumAMP-Activated Protein KinasesAnimalsMaleMiceMice, Inbred C57BLReceptor, Fibroblast Growth Factor, Type 1Signal TransductionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesFgfr1 protein, mousefibroblast growth factor 21Fibroblast Growth FactorsmTOR protein, mouseReceptor, Fibroblast Growth Factor, Type 1TOR Serine-Threonine KinasesFGF21FGFR1/AMPK/mTOR pathwayHepatorenal histopathologyIschemic strokeNeurologic deficitSalmonella typhimurium

Identifiers

PMID40581646
PMCPMC12205506

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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.