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. 2022 Sep 16;16:947295. doi: 10.3389/fnins.2022.947295

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Copyright © 2022 Zhou, He, Fan, Li, Zuo, Li, Gao and Sun.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential role of astrocytic endoplasmic reticulum (ER) stress and Toll-like receptor 4 (TLR4) signaling in obesity and inflammation. In hypothalamic astrocytes, ER stress may activate TLR4 that then activates myeloid differentiation primary response 88 (MyD88)-independent and MyD88-dependent signaling, which increases the expression of nuclear factor κB (NF-κB), mitogen-activated protein kinases (MAPKs), extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38. These effects upregulate pro-inflammatory cytokines such as interleukin 6 (IL-6), IL-1β, and tumor necrosis factor alpha (TNF-α), and causing central inflammation. Activated astrocytic TLR4 signaling could also lead to decreased energy expenditure and promote ER stress activation, which increases food intake, eventually leading to obesity.