Activation and Regulation of NLRP3 Inflammasome

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 November 2025) | Viewed by 927

Special Issue Editor

Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201301, China
Interests: inflammasome biology; innate immunity; inflammatory diseases; drug discovery; molecular pharmacology; cell signaling; pyroptosis; autophagy; metabolic regulation; therapeutic targeting

Special Issue Information

Dear Colleagues,

The NLRP3 inflammasome represents one of the most extensively studied innate immune complexes and plays a crucial role in the host defense against pathogens and cellular damage. However, dysregulation of NLRP3 inflammasome activation contributes to the pathogenesis of numerous inflammatory, metabolic, and neurodegenerative disorders. This Special Issue aims to compile cutting-edge research and comprehensive reviews focusing on the molecular mechanisms governing NLRP3 inflammasome activation, regulation, and its implications in health and disease.

We welcome original research articles and reviews that explore various aspects of NLRP3 inflammasome biology, including but not limited to structural insights into assembly and activation; novel regulatory mechanisms involving post-translational modifications; crosstalk with other cellular pathways such as autophagy, mitochondrial dynamics, and metabolic processes; roles in specific disease contexts; and innovative therapeutic strategies targeting the NLRP3 inflammasome. Emerging technologies for studying inflammasome dynamics and the development of selective NLRP3 inhibitors are also of particular interest.

By gathering diverse perspectives and recent advances in this rapidly evolving field, this Special Issue seeks to enhance our understanding of NLRP3 inflammasome biology and accelerate the development of targeted therapeutics for inflammasome-driven diseases.

Dr. Wei Guo
Guest Editor

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Keywords

  • NLRP3 inflammasome
  • innate immunity
  • inflammation
  • pyroptosis
  • caspase-1
  • IL-1β
  • IL-18
  • DAMPs
  • PAMPs
  • inflammasome inhibitors
  • post-translational modifications
  • chronic inflammatory diseases
  • metabolic disorders
  • neurodegenerative diseases
  • therapeutic targeting

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Published Papers (1 paper)

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Research

14 pages, 3360 KB  
Article
NLRP3-Mediated Neuroinflammation Participates in Resilience to PSD in C57BL/6 Mice
by Huikang Fu, Mengqing Xiong, Qi Xu, Xiaonan Liu, Xiaohui Chen, Ying Su and Zuotian Wu
Biomedicines 2026, 14(2), 297; https://doi.org/10.3390/biomedicines14020297 - 29 Jan 2026
Viewed by 690
Abstract
Background: Post-stroke depression (PSD) is a common complication of stroke, in which neuroinflammation plays a crucial role. Depression resilience has garnered significant attention in recent years, yet its relevance to PSD remains unexplored. Methods: In this study, we assessed emotional behaviors in C57BL/6 [...] Read more.
Background: Post-stroke depression (PSD) is a common complication of stroke, in which neuroinflammation plays a crucial role. Depression resilience has garnered significant attention in recent years, yet its relevance to PSD remains unexplored. Methods: In this study, we assessed emotional behaviors in C57BL/6 mice subjected to stereotaxic injection of endothelin-1 (ET1). Subsequently, hippocampal samples were collected to analyze the levels of NLRP3/NF-κB, along with microglial activation in the hippocampus. Results: The results showed that ET1 injection induced depressive-like behaviors in a subset of rodents. However, a subset of mice showed no statistically significant differences from the control group in measures from the open field test (OFT), elevated plus maze (EPM), tail suspension test (TST), and forced swim test (FST), demonstrating depression resilience to PSD. Furthermore, PSD animals exhibited activated microglia and NLRP3/NF-κB activation, whereas these markers in the resilient group showed no significant difference compared to controls. Conclusions: This study provides evidence that depression resilience exists in a PSD model, and it suggests that the microglia–NLRP3 signaling axis may participate in this resilient phenotype. These findings offer potential intervention targets for the clinical prevention and treatment of PSD. Full article
(This article belongs to the Special Issue Activation and Regulation of NLRP3 Inflammasome)
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