Evidence map›Paper›PMID 41910841›Full record

ArticleJournal of molecular neuroscience : MN2026

Circ-find-0001774 Modulates Parkinson's Disease via miR-153-3p: Mechanistic Insights and Therapeutic Implications.

Ronglan Zhu, Jie Chen, Tao Song, Yun Yang, Chaoyang Zhou, Zhiping Xie, Min Yuan, Jianzhong Zhang

Abstract read
In one paragraph

Article in Journal of molecular neuroscience : MN, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Ronglan Zhu *Department of Neurosurgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, No.266, Fenghe North Avenue, Honggutan District, Nanchang, 330038, Jiangxi, PR China.
Jie Chen *Department of Neurosurgery, Xiangya Hospital, Central South University, Jiangxi (National Regional Medical Center for Neurological Diseases), Nanchang, China.
Tao SongDepartment of Neurosurgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, No.266, Fenghe North Avenue, Honggutan District, Nanchang, 330038, Jiangxi, PR China.
Yun YangDepartment of Neurology, Xiangya Hospital, Central South University, Jiangxi(National Regional Medical Center for Neurological Diseases), Nanchang, China.
Chaoyang ZhouDepartment of Neurosurgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, No.266, Fenghe North Avenue, Honggutan District, Nanchang, 330038, Jiangxi, PR China.
Zhiping XieDepartment of Neurosurgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, No.266, Fenghe North Avenue, Honggutan District, Nanchang, 330038, Jiangxi, PR China.
Min YuanDepartment of Neurology, Xiangya Hospital, Central South University, Jiangxi(National Regional Medical Center for Neurological Diseases), Nanchang, China. yuanmin201314@sina.com.
Jianzhong ZhangDepartment of Neurosurgery, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, No.266, Fenghe North Avenue, Honggutan District, Nanchang, 330038, Jiangxi, PR China. zhangjianzhong@ncmc.edu.cn.

Funding

Jiangxi Provincial Education Department Science and Technology Program No:GJJ218908Jiangxi Provincial Health Technology Project No.202310113Jiangxi Provincial Natural Science Foundation No: 20242BAB25471
6 · The paper itself

Abstract

objectiveThis study aimed to investigate how circ-find-0001774 regulates miR-153-3p in Parkinson’s disease (PD).

methodsWe first validated the targeting relationship between circ-find-0001774 and miR-153-3p using dual-luciferase reporter assays, excluding any association with let-7a-5p. Next, we constructed a circ-find-0001774 overexpression vector and transfected it into MN9D dopaminergic neurons, confirming transfection efficiency by qPCR. In vitro, we induced a PD cell model with 100 µmol/L MPP+ iodide for 24 h and assessed cell proliferation using CCK-8, apoptosis via flow cytometry, and miR-153-3p and LC3Ⅱ/Ⅰ protein levels by qPCR and Western blotting. In vivo, we established a mouse PD model by daily intraperitoneal injection of 18 mg/kg MPTP for seven days, evaluating motor function through behavioral tests, observing brain pathology via HE staining, and analyzing miR-153-3p and β-catenin protein levels by qPCR and Western blotting.

resultsDual-luciferase assays confirmed a specific targeting interaction between miR-153-3p and circ-find-0001774. In vitro, circ-find-0001774 overexpression significantly enhanced cell proliferation, reduced apoptosis and decreased miR-153-3p and LC3Ⅱ/Ⅰ protein expression levels. In vivo, circ-find-0001774 overexpression notably ameliorated motor deficits in the mouse PD model mitigated neurodegeneration, decreased miR-153-3p level and increased β-catenin protein expression levels.

conclusionOur study reveals that circ-find-0001774 modulates miR-153-3p, mainly through the Wnt/β-Catenin signaling pathway, suggesting its therapeutic potential for PD. These findings provide novel insights and experimental foundations for further developing PD treatment strategies.

Indexed as

MicroRNAsParkinson DiseaseRNA, CircularAnimalsApoptosisbeta CateninCell LineCell ProliferationDopaminergic NeuronsHumansMaleMiceMice, Inbred C57BLbeta CateninMicroRNAsMIRN153 microRNA, humanMIRN153 microRNA, mouseRNA, Circularcirc-find-0001774Dopaminergic neuronsmiR-153-3pNeuroprotectionParkinson's diseaseWnt/β-Catenin signaling

Identifiers

PMID41910841
PMCPMC13035591

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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.