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miR-214-3p promotes the pathogenesis of Parkinson's disease by inhibiting autophagy.
Dong, Hui; Yan, Jiahui; Huang, Ping; Wang, Xinyu; Zhang, Ru; Zhang, Caiyun; Wang, Wenhui; Qian, Wenxian; Zhou, Jin; Zhao, Yunli; Gao, Jinghan; Zhang, Mengmeng; Ma, Xiuchang; Wang, Zhizhong; Yi, Changhua; Zhang, Jie; Chen, Wei.
Afiliação
  • Dong H; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China.
  • Yan J; Molecular Diagnostic Center, The Sixth Affiliated Hospital of Guangzhou Medical University/Qingyuan People's Hospital, Qingyuan 511518, China.
  • Huang P; Department of Hepatology, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China.
  • Wang X; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China.
  • Zhang R; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China.
  • Zhang C; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China.
  • Wang W; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China.
  • Qian W; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China.
  • Zhou J; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China.
  • Zhao Y; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China.
  • Gao J; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China.
  • Zhang M; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China.
  • Ma X; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China.
  • Wang Z; Henan Key Laboratory of Brain Science and Brain-Computer Interface Technology, School of Electrical and Information Engineering, Zhengzhou University, Zhengzhou 450001, China.
  • Yi C; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China. Electronic address: chhuayi@sina.cn.
  • Zhang J; Department of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, 70 President Street, DDB410, Charleston, SC 29425, USA. Electronic address: zhajie@musc.edu.
  • Chen W; Clinical Research Center, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210003, China; The Clinical Infectious Disease Center of Nanjing, Nanjing 210003, China. Electronic address: njyy039@njucm.edu.cn.
Biomed Pharmacother ; 171: 116123, 2024 Feb.
Article em En | MEDLINE | ID: mdl-38211424
ABSTRACT
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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doença de Parkinson / MicroRNAs Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doença de Parkinson / MicroRNAs Idioma: En Ano de publicação: 2024 Tipo de documento: Article