Evidence map›Paper›PMID 38802919›Full record

ArticleJournal of nanobiotechnology2024

Anti-ferroptosis exosomes engineered for targeting M2 microglia to improve neurological function in ischemic stroke.

Yong Wang, Zhuohang Liu, Luyu Li, Zengyu Zhang, Kai Zhang, Min Chu, Yang Liu, Xueyu Mao, Di Wu, Dongsheng Xu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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3 more citing papers are in PubMed but not listed here.

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

11 authors.

Yong Wang *Department of Neurology, Minhang Hospital, Fudan University, Shanghai, 201100, China.
Zhuohang Liu *Department of Neurology, Minhang Hospital, Fudan University, Shanghai, 201100, China.
Luyu Li *Department of Dermatology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200001, China.
Zengyu ZhangDepartment of Neurology, Minhang Hospital, Fudan University, Shanghai, 201100, China.
Kai ZhangDepartment of Cardiovascular Medicine, Pujiang Traditional Chinese Medicine Hospital, Zhejiang, 322200, China.
Min ChuDepartment of Neurology, Minhang Hospital, Fudan University, Shanghai, 201100, China.
Yang LiuDepartment of Neurology, Minhang Hospital, Fudan University, Shanghai, 201100, China.
Xueyu MaoDepartment of Neurology, Minhang Hospital, Fudan University, Shanghai, 201100, China.
Di WuDepartment of Neurology, Minhang Hospital, Fudan University, Shanghai, 201100, China.
Dongsheng XuCollege of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, 200120, China.
Jing ZhaoDepartment of Neurology, Minhang Hospital, Fudan University, Shanghai, 201100, China. zhao_jing@fudan.edu.cn.ORCID http://orcid.org/0000-0001-5197-9181

Funding

National Natural Science Foundation of China 81973157
6 · The paper itself

Abstract

backgroundStroke is a devastating disease affecting populations worldwide and is the primary cause of long-term disability. The inflammatory storm plays a crucial role in the progression of stroke. In the acute phase of ischemic stroke, there is a transient increase in anti-inflammatory M2 microglia followed by a rapid decline. Due to the abundant phospholipid in brain tissue, lipid peroxidation is a notable characteristic of ischemia/reperfusion (I/R), constituting a structural foundation for ferroptosis in M2 microglia. Slowing down the decrease in M2 microglia numbers and controlling the inflammatory microenvironment holds significant potential for enhancing stroke recovery.

resultsWe found that the ferroptosis inhibitor can modulate inflammatory response in MCAO mice, characterizing that the level of M2 microglia-related cytokines was increased. We then confirmed that different subtypes of microglia exhibit distinct sensitivities to I/R-induced ferroptosis. Adipose-derived stem cells derived exosome (ADSC-Exo) effectively decreased the susceptibility of M2 microglia to ferroptosis via Fxr2/Atf3/Slc7a11, suppressing the inflammatory microenvironment and promoting neuronal survival. Furthermore, through plasmid engineering, a more efficient M2 microglia-targeted exosome, termed M2pep-ADSC-Exo, was developed. In vivo and in vitro experiments demonstrated that M2pep-ADSC-Exo exhibits significant targeting specificity for M2 microglia, further inhibiting M2 microglia ferroptosis and improving neurological function in ischemic stroke mice.

conclusionCollectively, we illustrated a novel potential therapeutic mechanism that Fxr2 in ADSC-Exo could alleviate the M2 microglia ferroptosis via regulating Atf3/Slc7all expression, hence inhibiting the inflammatory microenvironment, improving neurofunction recovery in cerebral I/R injury. We obtained a novel exosome, M2pep-ADSC-Exo, through engineered modification, which exhibits improved targeting capabilities toward M2 microglia. This provides a new avenue for the treatment of stroke.

Indexed as

ExosomesFerroptosisIschemic StrokeMice, Inbred C57BLMicrogliaAmino Acid Transport System y+AnimalsBrain IschemiaCytokinesDisease Models, AnimalMaleMiceAmino Acid Transport System y+CytokinesSlc7a11 protein, mouseEngineered exosomesFerroptosis susceptibilityInflammatory microenvironmentIschemic strokeLipid peroxidationM2 microglia

Identifiers

PMID38802919
PMCPMC11129432

What OpenQuestion holds

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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 OpenQuestion graph.