ReviewFrontiers in aging neuroscience2025
Autophagy-mediated regulation of neutrophil inflammatory responses and its relevance to central nervous system diseases.
Review in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
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.
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