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[Pathogenic mechanisms of impaired neuronal autophagy flux after ischemic stroke].
Liu, Ji-Yu; He, Hong-Yun; Deng, Yi-Hao.
Afiliação
  • Liu JY; Department of Human Anatomy, Faculty of Medicine, Kunming University of Science and Technology, Kunming 650500, China.
  • He HY; Department of Human Anatomy, Faculty of Medicine, Kunming University of Science and Technology, Kunming 650500, China.
  • Deng YH; Anning First People's Hospital Affiliated to Kunming University of Science and Technology, Kunming 650399, China. 20130211@kust.edu.cn.
Sheng Li Xue Bao ; 76(1): 97-104, 2024 Feb 25.
Article em Zh | MEDLINE | ID: mdl-38444135
ABSTRACT
Autophagy is a metabolic process in which damaged organelles, obsolete proteins, excess cytoplasmic components, and even pathogens are presented to lysosomes for degradation via autophagosomes. It includes 4 processes the initiation of autophagy, the formation of autophagosomes, the fusion of autophagosomes with lysosomes, and the degradation and removal of autophagic substrates within autophagic lysosomes. When these processes are continuous, it is called autophagy flux. Blockage of one or certain steps in the autophagy/lysosome signaling pathway can lead to impaired autophagy flux. Numerous studies have shown that impaired autophagy flux is an important cause of neuronal damage in the ischemic penumbra after stroke. This paper summarized research progress in the pathological mechanisms that cause impaired neuronal autophagy flux after ischemic stroke and discusses methods to improve neuronal autophagy flux, in order to provide a reference for an in-depth investigation of the pathological injury mechanisms after stroke.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Acidente Vascular Cerebral / AVC Isquêmico Limite: Humans Idioma: Zh Ano de publicação: 2024 Tipo de documento: Article
Buscar no Google
Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Acidente Vascular Cerebral / AVC Isquêmico Limite: Humans Idioma: Zh Ano de publicação: 2024 Tipo de documento: Article