Epigenetic regulation of autophagy in neuroinflammation and synaptic plasticity

Autophagy is a conserved cellular mechanism that enables the degradation and recycling of cellular organelles and proteins the lysosomal pathway. In neurodevelopment and maintenance of neuronal homeostasis, autophagy is required to regulate presynaptic functions, synapse remodeling, and synaptic pla...

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Published in:Frontiers in immunology 2024-02, Vol.15, p.1322842
Main Authors: Bai, Isaac, Keyser, Cameron, Zhang, Ziyan, Rosolia, Breandan, Hwang, Jee-Yeon, Zukin, R Suzanne, Yan, Jingqi
Format: Article
Language:English
Subjects:
autophagy
Autophagy - genetics
Epigenesis, Genetic
epigenetics
Humans
Immunology
microglia
neuroinflammation
Neuroinflammatory Diseases
Neuronal Plasticity - genetics
Neurons - metabolism
synapse
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Summary:Autophagy is a conserved cellular mechanism that enables the degradation and recycling of cellular organelles and proteins the lysosomal pathway. In neurodevelopment and maintenance of neuronal homeostasis, autophagy is required to regulate presynaptic functions, synapse remodeling, and synaptic plasticity. Deficiency of autophagy has been shown to underlie the synaptic and behavioral deficits of many neurological diseases such as autism, psychiatric diseases, and neurodegenerative disorders. Recent evidence reveals that dysregulated autophagy plays an important role in the initiation and progression of neuroinflammation, a common pathological feature in many neurological disorders leading to defective synaptic morphology and plasticity. In this review, we will discuss the regulation of autophagy and its effects on synapses and neuroinflammation, with emphasis on how autophagy is regulated by epigenetic mechanisms under healthy and diseased conditions.
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2024.1322842