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小胶质细胞在稳态和高脂饮食诱导的炎症状态下调节神经元回路。

Microglia Regulate Neuronal Circuits in Homeostatic and High-Fat Diet-Induced Inflammatory Conditions.

作者信息

Wang Xiao-Lan, Li Lianjian

机构信息

Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Department of Surgery, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China.

出版信息

Front Cell Neurosci. 2021 Oct 13;15:722028. doi: 10.3389/fncel.2021.722028. eCollection 2021.

DOI:10.3389/fncel.2021.722028
PMID:34720877
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8549960/
Abstract

Microglia are brain resident macrophages, which actively survey the surrounding microenvironment and promote tissue homeostasis under physiological conditions. During this process, microglia participate in synaptic remodeling, neurogenesis, elimination of unwanted neurons and cellular debris. The complex interplay between microglia and neurons drives the formation of functional neuronal connections and maintains an optimal neural network. However, activation of microglia induced by chronic inflammation increases synaptic phagocytosis and leads to neuronal impairment or death. Microglial dysfunction is implicated in almost all brain diseases and leads to long-lasting functional deficiency, such as hippocampus-related cognitive decline and hypothalamus-associated energy imbalance (i.e., obesity). High-fat diet (HFD) consumption triggers mediobasal hypothalamic microglial activation and inflammation. Moreover, HFD-induced inflammation results in cognitive deficits by triggering hippocampal microglial activation. Here, we have summarized the current knowledge of microglial characteristics and biological functions and also reviewed the molecular mechanism of microglia in shaping neural circuitries mainly related to cognition and energy balance in homeostatic and diet-induced inflammatory conditions.

摘要

小胶质细胞是脑内常驻巨噬细胞,在生理条件下,它们积极监测周围微环境并促进组织稳态。在此过程中,小胶质细胞参与突触重塑、神经发生、清除不需要的神经元和细胞碎片。小胶质细胞与神经元之间复杂的相互作用驱动功能性神经元连接的形成,并维持最佳神经网络。然而,慢性炎症诱导的小胶质细胞激活会增加突触吞噬作用,并导致神经元损伤或死亡。小胶质细胞功能障碍几乎与所有脑部疾病有关,并导致长期的功能缺陷,如与海马体相关的认知衰退和与下丘脑相关的能量失衡(即肥胖)。高脂饮食(HFD)会引发下丘脑内侧基底部小胶质细胞的激活和炎症。此外,高脂饮食诱导的炎症通过触发海马体小胶质细胞激活导致认知缺陷。在此,我们总结了小胶质细胞特征和生物学功能的现有知识,并回顾了在稳态和饮食诱导的炎症条件下,小胶质细胞在塑造主要与认知和能量平衡相关的神经回路中的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc6/8549960/0c84a7a0e70d/fncel-15-722028-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc6/8549960/0c84a7a0e70d/fncel-15-722028-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc6/8549960/0c84a7a0e70d/fncel-15-722028-g001.jpg

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