miR-214-3p promotes the pathogenesis of Parkinson's disease by inhibiting autophagy

Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved..

Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by dopaminergic neuron death in the substantia nigra, leading to motor dysfunction. Autophagy dysregulation has been implicated in PD pathogenesis. This study explores the role of miR-214-3p in PD, focusing on its impact on autophagy and dopaminergic neuron viability. Using in vitro and in vivo models, we demonstrate that miR-214-3p inhibits autophagy and promotes dopaminergic neuron apoptosis. Behavioral assessments and molecular analyses reveal exacerbation of PD symptoms upon miR-214-3p overexpression. Furthermore, mechanistic investigations identify ATG3 as a target, shedding light on miR-214-3p's regulatory role in autophagy. These findings enhance our understanding of PD pathogenesis and propose miR-214-3p as a potential biomarker and therapeutic target for modulating autophagy and neuronal survival in PD.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:171

Enthalten in:

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie - 171(2024) vom: 07. Feb., Seite 116123

Sprache:

Englisch

Beteiligte Personen:

Dong, Hui [VerfasserIn]
Yan, Jiahui [VerfasserIn]
Huang, Ping [VerfasserIn]
Wang, Xinyu [VerfasserIn]
Zhang, Ru [VerfasserIn]
Zhang, Caiyun [VerfasserIn]
Wang, Wenhui [VerfasserIn]
Qian, Wenxian [VerfasserIn]
Zhou, Jin [VerfasserIn]
Zhao, Yunli [VerfasserIn]
Gao, Jinghan [VerfasserIn]
Zhang, Mengmeng [VerfasserIn]
Ma, Xiuchang [VerfasserIn]
Wang, Zhizhong [VerfasserIn]
Yi, Changhua [VerfasserIn]
Zhang, Jie [VerfasserIn]
Chen, Wei [VerfasserIn]

Links:

Volltext

Themen:

ATG3
Autophagy
Dopaminergic neurons
Journal Article
MIRN214 microRNA, human
MiR-214–3p
MicroRNAs
Parkinson's disease

Anmerkungen:

Date Completed 08.02.2024

Date Revised 08.02.2024

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1016/j.biopha.2024.116123

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM367019736