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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Psychiatry. Aug 19, 2026; 16(8): 120501
Published online Aug 19, 2026. doi: 10.5498/wjp.120501
Nuclear factor-κB as a key inflammatory mediator in psychiatric diseases: A narrative review
Fei Fan, Bo Wang, Qiong Wang, Zi-Lin Chen, Wei-Feng Li, Fei Han
Fei Fan, Bo Wang, Qiong Wang, Zi-Lin Chen, Wei-Feng Li, Fei Han, Department of Paediatrics, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China
Author contributions: Chen ZL, Li WF and Fan F led analysis and writing of the manuscript; Fan F and Wang B performed experimental operations; Wang Q and Han F supervised the research. All authors read and approved the final manuscript.
AI contribution statement: AI tools (specifically Paperpal) were used solely for linguistic refinement and formatting assistance. No AI tool was involved in the generation of research data, interpretation of results, or formulation of conclusions. All AI-generated outputs were critically reviewed and revised by the authors.
Supported by the Fundamental Research Funds for the Central Public Welfare Research Institutes, No. ZZ17-XRZ-043.
Conflict-of-interest statement: The authors declare no conflict of interest.
Corresponding author: Fei Han, Department of Paediatrics, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, No. 5 Beixiange Road, Xicheng District, Beijing 100053, China. hf4383@126.com
Received: February 28, 2026
Revised: March 21, 2026
Accepted: May 6, 2026
Published online: August 19, 2026
Processing time: 139 Days and 17.7 Hours
Core Tip

Core Tip: Nuclear factor-κB (NF-κB) is a central transcription factor linking peripheral immune dysregulation to neuroinflammation in psychiatric disorders. It exerts cell-type-specific effects on microglia, astrocytes, and neurons, interacting with nuclear factor erythroid 2-related factor 2, hypoxia-inducible factor 1-alpha, and NOD-like receptor family pyrin domain containing 3 pathways. Targeting NF-κB and its regulators offers promising therapeutic potential for personalized psychiatry.

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