The regulatory mechanism of NLRP3 inflammasome in the "immune paralytic-overactivation" imbalance in sepsis: the latest progress from molecular signaling to clinical translation.

Authors

Gaosheng Zhou, Yifei Chen, Dingdeng Wang, Yixin Cheng, Zhaohui Zhang

Published in

Frontiers in immunology. Volume 17. Pages 1751283. Epub Apr 30, 2026.

Abstract

Sepsis remains a major challenge in critical care medicine worldwide, characterized by a dynamic imbalance of the immune system between two extremes: "immunoparalysis" and "hyperactivation." This dysregulation severely affects patient survival. The NLRP3 inflammasome, a central molecular platform in innate immunity, has recently been shown to play a critical dual role in the pathogenesis of sepsis. This review systematically outlines the structural features and activation mechanisms of the NLRP3 inflammasome, elaborates on its pro-inflammatory and immunosuppressive effects in sepsis-induced immune dysregulation, and summarizes the associated signaling pathways and regulatory networks. By integrating recent advances in basic and clinical research, we provide an in-depth analysis of the molecular regulatory mechanisms of the NLRP3 inflammasome in sepsis and evaluate its potential as a therapeutic target. Furthermore, this review discusses the opportunities and challenges in translating NLRP3-targeted strategies into clinical practice, emphasizing the potential of precise NLRP3 modulation to restore immune homeostasis in sepsis. Our findings may provide a theoretical foundation and future research directions for developing novel therapeutic approaches.

PMID:
42148064
Bibliographic data and abstract were imported from PubMed on 15 Sep 2026.

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