Evidence map›Paper›PMID 38200351›Full record

ArticleMolecular neurobiology2024

MSC-Derived Extracellular Vesicles Alleviate NLRP3/GSDMD-Mediated Neuroinflammation in Mouse Model of Sporadic Alzheimer's Disease.

Lishan Lin, Longxin Huang, Sen Huang, Weineng Chen, Heng Huang, Li Chi, Fengjuan Su, Xiaoqing Liu, Kang Yuan, Qiuhong Jiang and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
–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

25 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

14 authors.

Lishan Lin *Department of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases; National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, Guangzhou, 510080, China.
Longxin Huang *Otorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China.
Sen Huang *Department of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases; National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, Guangzhou, 510080, China.
Weineng ChenDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases; National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, Guangzhou, 510080, China.
Heng HuangDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Li ChiHospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Institute of Stomatology, Guanghua School of Stomatology, Sun Yat-Sen University, Guangzhou, 510080, China.
Fengjuan SuDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases; National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, Guangzhou, 510080, China.
Xiaoqing LiuOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China.
Kang YuanDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases; National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, Guangzhou, 510080, China.
Qiuhong JiangDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases; National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, Guangzhou, 510080, China.
Changu LiOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China.
Wanli W SmithDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Qingling FuOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China. fuqingl@mail.sysu.edu.cn.
Zhong PeiDepartment of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases; National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, Guangzhou, 510080, China. peizhong@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-7986-3452

Funding

Key Technologies Research and Development Program 2022YFA1104900National Natural Science Foundation of China 81970863National Natural Science Foundation of China 82071255National Natural Science Foundation of China 82271144National Natural Science Foundation of China 82271266
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease, with sporadic form being the predominant type. Neuroinflammation plays a critical role in accelerating pathogenic processes in AD. Mesenchymal stem cell (MSC)-derived small extracellular vesicles (MSC-sEVs) regulate inflammatory responses and show great promise for treating AD. Induced pluripotent stem cell (iPSC)-derived MSCs are similar to MSCs and exhibit low immunogenicity and heterogeneity, making them promising cell sources for clinical applications. This study examined the anti-inflammatory effects of MSC-sEVs in a streptozotocin-induced sporadic mouse model of AD (sAD). The intracisternal administration of iPSC-MSC-sEVs alleviated NLRP3/GSDMD-mediated neuroinflammation, decreased amyloid deposition and neuronal apoptosis, and mitigated cognitive dysfunction. Furthermore, it explored the role of miR-223-3p in the iPSC-MSC-sEVs-mediated anti-inflammatory effects in vitro. miR-223-3p directly targeted NLRP3, whereas inhibiting miR-223-3p almost completely reversed the suppression of NLRP3 by MSC-sEVs, suggesting that miR-223-3p may, at least partially, account for MSC-sEVs-mediated anti-inflammation. Results obtained suggest that intracisternal administration of iPSC-MSC-sEVs can reduce cognitive impairment by inhibiting NLRP3/GSDMD neuroinflammation in a sAD mouse model. Therefore, the present study provides a proof-of-principle for applying iPSC-MSC-sEVs to target neuroinflammation in sAD.

Indexed as

Alzheimer DiseaseDisease Models, AnimalExtracellular VesiclesMesenchymal Stem CellsMicroRNAsNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsInduced Pluripotent Stem CellsInflammationMiceMice, Inbred C57BLNeuroinflammatory DiseasesMicroRNAsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseAlzheimer diseaseMesenchymal stem cellNeuroinflammationNLRP3

Identifiers

PMID38200351

What OpenQuestion holds

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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.