HMGB1 in depression: An overview of microglial HMBG1 in the pathogenesis of depression

Huang, Xiao; Wang, Bo; Yang, Jing; Lian, Yong-Jie; Yu, Hong-Zhang; Wang, Yun-Xia

doi:10.1016/j.bbih.2023.100641

Cited by 6 publications

(1 citation statement)

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“…One of the DAMPs released from microglia by stress exposure (sterile inflammation) is the high-mobility group box 1 (HMGB1) [ 141 , 142 , 143 ]. HMGB1 can act via activation of Toll-like receptor 4 (TLR4) or Receptor for Advanced Glycation End Product (RAGE) in microglia, resulting in the release of several inflammatory mediators [ 144 ].…”

Section: Nnos No-related Mechanisms and Stress Responsementioning

confidence: 99%

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

Fronza,

Ferreira,

Pavan-Silva

et al. 2023

Molecules

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Post-traumatic stress disorder (PTSD) is a psychiatric condition characterized by persistent fear responses and altered neurotransmitter functioning due to traumatic experiences. Stress predominantly affects glutamate, a neurotransmitter crucial for synaptic plasticity and memory formation. Activation of the N-Methyl-D-Aspartate glutamate receptors (NMDAR) can trigger the formation of a complex comprising postsynaptic density protein-95 (PSD95), the neuronal nitric oxide synthase (nNOS), and its adaptor protein (NOS1AP). This complex is pivotal in activating nNOS and nitric oxide (NO) production, which, in turn, activates downstream pathways that modulate neuronal signaling, including synaptic plasticity/transmission, inflammation, and cell death. The involvement of nNOS and NOS1AP in the susceptibility of PTSD and its comorbidities has been widely shown. Therefore, understanding the interplay between stress, fear, and NO is essential for comprehending the maintenance and progression of PTSD, since NO is involved in fear acquisition and extinction processes. Moreover, NO induces post-translational modifications (PTMs), including S-nitrosylation and nitration, which alter protein function and structure for intracellular signaling. Although evidence suggests that NO influences synaptic plasticity and memory processing, the specific role of PTMs in the pathophysiology of PTSD remains unclear. This review highlights pathways modulated by NO that could be relevant to stress and PTSD.

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