REVIEW article
Front. Aging Neurosci.
Sec. Neuroinflammation and Neuropathy
Autophagy-Mediated Regulation of Neutrophil Inflammatory Responses and Its Relevance to Central Nervous System Diseases
Provisionally accepted
- 1Department of Pharmacy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
- 2State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China
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Autophagy is an intracellular degradation system, which plays a crucial role in regulating the inflammatory functions of neutrophils. Neutrophils, as crucial immunological phagocytes, are integral to inflammatory responses. In central nervous system diseases, neutrophils' malfunction is closely associated with disease progression. Autophagy in neutrophils is highly conserved and plays a crucial regulatory role in both the biological functions and pathophysiological processes of neutrophils. In this review, we comprehensively explore the mechanisms of autophagy and its regulatory roles in various aspects of neutrophil biology, including the neutrophil life cycle, extracellular net traps (NETs) formation, degranulation, migration and adhesion, and phagocytosis. We also analyze the role of neutrophil autophagy in different central nervous system diseases such as Alzheimer's disease, stroke, and neuroglioma. Regulating autophagy to control neutrophil inflammatory functions may emerge as a novel therapeutic strategy for treating central nervous system disorders.
Keywords: Autophagy, Neutrophil, Inflammation, Central Nervous System Diseases, NETs
Received: 11 Sep 2025; Accepted: 25 Nov 2025.
Copyright: © 2025 Li, Tan and Zuo. 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) or licensor 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.
* Correspondence: Wei Zuo
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.