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Reprogramming of astrocytes and glioma cells into neurons for central nervous system repair and glioblastoma therapy.
Wei, Junyuan; Wang, Miaomiao; Li, Shilin; Han, Rui; Xu, Wenhong; Zhao, Anqi; Yu, Qi; Li, Haokun; Li, Meiying; Chi, Guangfan.
Afiliação
  • Wei J; The Key Laboratory of Pathobiology, Ministry of Education, and College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address: jywei22@mails.jlu.edu.cn.
  • Wang M; The Key Laboratory of Pathobiology, Ministry of Education, and College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address: mmwang22@mails.jlu.edu.cn.
  • Li S; School of Public Health, Jilin University, Changchun 130021, China. Electronic address: lisl2720@mails.jlu.edu.cn.
  • Han R; Department of Neurovascular Surgery, First Hospital of Jilin University, 1xinmin Avenue, Changchun, Jilin Province 130021, China. Electronic address: hanrui.jlu@foxmail.com.
  • Xu W; The Key Laboratory of Pathobiology, Ministry of Education, and College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address: whxu20@jlu.edu.cn.
  • Zhao A; The Key Laboratory of Pathobiology, Ministry of Education, and College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address: zhaoaq21@mails.jlu.edu.cn.
  • Yu Q; The Key Laboratory of Pathobiology, Ministry of Education, and College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address: qyu21@mails.jlu.edu.cn.
  • Li H; The Key Laboratory of Pathobiology, Ministry of Education, and College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address: lihk23@mails.jlu.edu.cn.
  • Li M; The Key Laboratory of Pathobiology, Ministry of Education, and College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address: limeiying@jlu.edu.cn.
  • Chi G; The Key Laboratory of Pathobiology, Ministry of Education, and College of Basic Medical Sciences, Jilin University, Changchun 130021, China. Electronic address: guangfan130@jlu.edu.cn.
Biomed Pharmacother ; 176: 116806, 2024 Jul.
Article em En | MEDLINE | ID: mdl-38796971
ABSTRACT
Central nervous system (CNS) damage is usually irreversible owing to the limited regenerative capability of neurons. Following CNS injury, astrocytes are reactively activated and are the key cells involved in post-injury repair mechanisms. Consequently, research on the reprogramming of reactive astrocytes into neurons could provide new directions for the restoration of neural function after CNS injury and in the promotion of recovery in various neurodegenerative diseases. This review aims to provide an overview of the means through which reactive astrocytes around lesions can be reprogrammed into neurons, to elucidate the intrinsic connection between the two cell types from a neurogenesis perspective, and to summarize what is known about the neurotranscription factors, small-molecule compounds and MicroRNA that play major roles in astrocyte reprogramming. As the malignant proliferation of astrocytes promotes the development of glioblastoma multiforme (GBM), this review also examines the research advances on and the theoretical basis for the reprogramming of GBM cells into neurons and discusses the advantages of such approaches over traditional treatment modalities. This comprehensive review provides new insights into the field of GBM therapy and theoretical insights into the mechanisms of neurological recovery following neurological injury and in GBM treatment.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Encefálicas / Astrócitos / Glioblastoma / Reprogramação Celular / Neurônios Limite: Animals / Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Encefálicas / Astrócitos / Glioblastoma / Reprogramação Celular / Neurônios Limite: Animals / Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article