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Pathogenic mechanisms of impaired neuronal autophagy flux after ischemic stroke

LIU Ji-Yu¹, HE Hong-Yun^1,2, DENG Yi-Hao^1,*

¹Department of Human Anatomy, Faculty of Medicine, Kunming University of Science and Technology, Kunming 650500, China；²Anning First People’s Hospital Affiliated to Kunming University of Science and Technology, Kunming 650399, China

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.

Key words: autophagy; ischemic stroke; autophagic lysosomes; autophagic flow disorders; pathological mechanisms

Received: 　　Accepted:

Corresponding author: 邓仪昊　　E-mail: 20130117@kust.edu.cn

DOI: 10.13294/j.aps.2024.0004

Citing This Article：

LIU Ji-Yu, HE Hong-Yun, DENG Yi-Hao. Pathogenic mechanisms of impaired neuronal autophagy flux after ischemic stroke. Acta Physiol Sin 2024; 76 (1): 97-104 (in Chinese with English abstract).