Interactions between neutrophil extracellular traps (NETs) and macrophages play a critical role in the initiation and progression of inflammatory diseases. NETs regulate macrophage polarization and function by releasing components such as DNA, histones, and granule proteins, as well as by activating multiple signaling pathways. In turn, macrophages modulate the formation and clearance of NETs through the secretion of cytokines and proteases. This bidirectional interaction forms a positive feedback loop in autoimmune diseases, cardiovascular diseases, and the tumor microenvironment, exacerbating inflammatory responses and tissue injury. Investigating the specific mechanisms underlying the NETs–macrophage interplay may provide novel targeted therapeutic strategies for inflammatory diseases. Therefore, this article systematically reviews the mechanisms of NETs–macrophage interactions and their pathological roles in various inflammatory diseases, aiming to offer a theoretical foundation and translational potential for future research.
Shan et al. (Fri,) studied this question.
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