Evidence map›Paper›PMID 42176037›Full record

ArticleNeurochemical research2026

Lipid Nanoparticle-Delivered Circ_0017866 Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing Endothelial-Mesenchymal Transition via the miR-124-3p/CLDND1 Axis.

Yuzhen Wang, Yaozhuo Cai, Xuan Zhang, Dandan Wang, Bailong Xin, Xueli Cai, Jingping Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

7 authors.

Yuzhen Wang *Department of Neurology, Lishui Central Hospital, The Fifth Affiliated Hospital of Wenzhou Medical University, 289 Kuocang Street, Lishui, 323000, Zhejiang Province, China.
Yaozhuo Cai *Department of Neurology, Lishui Central Hospital, The Fifth Affiliated Hospital of Wenzhou Medical University, 289 Kuocang Street, Lishui, 323000, Zhejiang Province, China.
Xuan ZhangDepartment of Neurology, Lishui Central Hospital, The Fifth Affiliated Hospital of Wenzhou Medical University, 289 Kuocang Street, Lishui, 323000, Zhejiang Province, China.
Dandan WangDepartment of Neurology, Lishui Central Hospital, The Fifth Affiliated Hospital of Wenzhou Medical University, 289 Kuocang Street, Lishui, 323000, Zhejiang Province, China.
Bailong XinLishui Clinical Research Center for Neurological Diseases, 289 Kuocang Street, Lishui, 323000, Zhejiang Province, China.
Xueli CaiDepartment of Neurology, Lishui Central Hospital, The Fifth Affiliated Hospital of Wenzhou Medical University, 289 Kuocang Street, Lishui, 323000, Zhejiang Province, China.
Jingping SunDepartment of Neurology, Lishui Central Hospital, The Fifth Affiliated Hospital of Wenzhou Medical University, 289 Kuocang Street, Lishui, 323000, Zhejiang Province, China. lszxyysunjingping@yeah.net.

Funding

the Zhejiang Provincial Basic Public Welfare Research Program Self-funded Project 2022SJGYZC02
6 · The paper itself

Abstract

Ischemic stroke poses a severe threat to human health, and cerebral ischemia-reperfusion injury (CIRI) following recanalization remains a critical challenge for patient prognosis. This study investigated the role and mechanism of the circ_0017866/miR-124-3p/claudin domain containing 1 (CLDND1) axis in CIRI-induced endothelial-mesenchymal transition (EndMT) and evaluated the therapeutic potential of lipid nanoparticle (LNP)-encapsulated circ_0017866. Both oxygen-glucose deprivation/reperfusion cell and middle cerebral artery occlusion/reperfusion mouse models were established. Molecular interactions and gene/protein expression were validated using dual-luciferase reporter assays, quanti-tative real-time PCR, western blot, and immunofluorescence. In vitro, endothelial cell viability and function were assessed through CCK-8, Transwell migration, and tube formation assays. In vivo, LNP-mediated delivery of circ_0017866 was employed, and neurological deficits and cerebral infarct volume were evaluated using modified neu-rological severity scores and 2,3,5-triphenyltetrazolium chloride staining. Both in vivo and in vitro studies demonstrated that after ischemia-reperfusion, the expression of circ_0017866 and CLDND1 was downregulated, while miR-124-3p expression was upregulated. The dual-luciferase assay confirmed that miR-124-3p directly targets both circ_0017866 and CLDND1. In the OGD/R model, either circ_0017866 overexpression or miR-124-3p inhibition upregulated the expression of CLDND1 and occludin, downregulated α-smooth muscle actin (α-SMA) and Snail, and improved endothelial function. In the MCAO/R model, LNP-circ_0017866 treatment significantly improved neurological deficits, reduced infarct volume, and decreased the abnormal expression of EndMT-related markers. Circ_0017866 alleviates CIRI-induced EndMT by functioning as a molecular sponge for miR-124-3p to indirectly regulate CLDND1 expression. LNP-delivered circ_0017866 effectively mitigates neurological deficits and reduces cerebral infarct volume, providing a promising therapeutic strategy for ischemic stroke.

Indexed as

Brain IschemiaEndothelial-Mesenchymal TransitionMicroRNAsNanoparticlesReperfusion InjuryRNA, CircularAnimalsHumansInfarction, Middle Cerebral ArteryLipidsMaleMiceMice, Inbred C57BLLipidsMicroRNAsMirn124 microRNA, mouseRNA, CircularCerebral ischemia-reperfusion injurycirc_0017866CLDND1Endothelial-mesenchymal transitionLipid nanoparticlemiR-124-3p

Identifiers

PMID42176037

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Registered trials

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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.